Myocardial Infarction – Carbon Chemist

October 30, 2024

Cancer history raises cardiovascular disease risk in hypertensive patients

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A study published in the journal Hypertension Research reveals that having a cancer history can increase the risk of cardiovascular disease in individuals with hypertension.

Study: Risk of cancer history in cardiovascular disease among individuals with hypertension. Image Credit: Black Salmon / Shutterstock

Background

A growing pool of evidence highlights the link between hypertension and cancer since both hypertension and cancer risks increase with advancing age, and that certain anti-cancer medications increase the risk of hypertension.

Several epidemiological studies have found that hypertension can increase the risk of certain types of cancers and that individuals with a cancer history are more likely to develop cardiovascular complications.

Given the potential link between the risks of hypertension, cardiovascular disease, and cancer, the scientists in this study have assessed the risk of cardiovascular disease events in hypertensive individuals with a history of cancer.

Study design

The study population included 747,620 individuals who were diagnosed with hypertension between January 2005 and May 2022. Patient information was collected from the JMDC Claims Database, a nationwide healthcare database in Japan.

Appropriate statistical analyses were conducted to determine the risk of Composite cardiovascular disease events, including myocardial infarction, angina pectoris, stroke, heart failure, and atrial fibrillation, based on the participant’s history of cancer and chemotherapy.

A history of cancer was defined as being diagnosed with malignancies before the initial health check-up.

Self-reported information on comorbidities (obesity, diabetes, and dyslipidemia), alcohol intake and smoking status, and physical activity level was collected from participants during the health check-up.

Important observations

A total of 26,531 individuals with a history of cancer were identified from the entire study population of 747,620 participants with hypertension. Participants with a history of cancer were more likely to be older adults, less likely to be men, and more likely to have diabetes. In contrast, participants without a history of cancer were more likely to have obesity and current smoking status.

A total of 67,154 composite cardiovascular disease events were detected during the study follow-up period until May 2022. Hypertensive patients with a history of cancer showed a significantly higher risk of developing composite cardiovascular disease events. However, the risk of developing myocardial infarction was not statistically significant.

The highest risk of developing cardiovascular disease events except myocardial infarction was observed among cancer survivors who received chemotherapy compared to those who did not receive chemotherapy or those without a history of cancer.

Regarding myocardial infarction, a higher risk was observed among cancer patients receiving chemotherapy compared to those without a history of cancer.

Five types of cancers, including colorectal cancer, prostate cancer, stomach cancer, renal, pelvic, and ureteral cancer, and lung cancer, showed the highest prevalence in men. In women, the highest prevalence was observed for breast cancer, colorectal cancer, thyroid cancer, corpus uteri cancer, and cervix uteri cancer.

A significantly higher risk of composite cardiovascular events was observed among men with a history of lung cancer and women with a history of breast cancer compared to those without a history of cancer.

A sensitivity analysis conducted after adjusting for age, sex, smoking status, alcohol intake, and physical inactivity showed a similar positive association between having a cancer history and risk of composite cardiovascular disease events.

Study significance

The study finds that hypertensive patients with a history of cancer have a higher risk of developing various cardiovascular disease events than those without a history of cancer. The risk of cardiovascular disease events is even higher in cancer patients receiving chemotherapy.

The study findings highlight the need for early screening of cancer in patients with hypertension. Physicians should manage hypertensive individuals more carefully as cancer comorbidity not only adversely affects cancer mortality but also significantly increases the risk of cardiovascular disease.

The coexistence of cancer and hypertension is a significant public health crisis in Asian countries. Implementation of appropriate healthcare policies is needed to prevent detrimental cardiovascular health consequences, particularly in developing countries with advanced aging.

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April 26, 2024

Younger adults with atrial fibrillation face higher rates of heart failure and stroke

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In a recent study published in the Circulation: Arrhythmia and Electrophysiology, a group of researchers investigated the risk factor (RF) burden, clinical outcomes, and long-term survival among patients with atrial fibrillation (AF) under 65 years of age.

Study: Mortality, Hospitalization, and Cardiac Interventions in Patients With Atrial Fibrillation Aged <65 Years. Image Credit: Nakharin T/Shutterstock.com

Background

AF, the most prevalent heart rhythm disorder in the United States (U.S.), affected an estimated 5.2 million people in 2010, with projections rising to 12.1 million by 2030.

While AF is typically seen in older adults, a growing number of patients are under 65 at diagnosis, representing 10%-15% of cases. This age group faces increasing rates of RFs, such as hypertension, diabetes, and obesity.

Despite their prevalence, the impact of AF on mortality and major clinical events in younger patients remains poorly defined. Further research is needed to clarify the unique clinical outcomes and effective management strategies for younger patients with AF.

About the study

The present study was a retrospective observational cohort analysis at the University of Pittsburgh Medical Center involving patients over 18 years diagnosed with AF.

The diagnosis was confirmed using the International Classification of Diseases (ICD), Ninth and Tenth Revision codes. Patients evaluated between January 2010 and December 2019, were included if they had at least two outpatient visits in internal medicine, family medicine, or cardiology.

Data were extracted from an extensive electronic health record system combined with administrative and other data sources.

This study assessed a range of cardiovascular risk factors and comorbidities, including obesity, smoking history, hypertension, diabetes, and various heart conditions. Detailed information on patient characteristics such as age, gender, and race was gathered, along with data on previous cardiovascular interventions and medication usage at baseline.

The primary outcome measured was all-cause mortality, verified through the Social Security Death Index and supplemented by electronic health record data. The study also looked at secondary outcomes like hospitalizations for cardiovascular events and cardiac interventions that occurred during follow-up.

Statistical analyses involved various tests to compare continuous and categorical variables and utilized Kaplan-Meier survival analysis and Cox proportional hazards models to explore the impact of AF on mortality in patients under 65, adjusting for multiple confounders.

Sensitivity analyses were conducted to consider the effects of various exclusions on the study results.

Study results

The study included 67,221 patients diagnosed with AF, reflecting an average CHA₂DS₂-VASc score of 3.1±1.6. The cohort’s average age was 72.4±12.3 years, with 45% female and 95% white participants. Notably, a significant portion, 26%, were under 65 years at their initial evaluation.

Within the subgroup of patients younger than 65, males were more prevalent, especially in those under 50 (73%) and those between 50 to 65 years (66.3%). This group displayed substantial cardiovascular RFs, including hypertension (55%), diabetes (21%), heart failure (HF) (21%), and dyslipidemia (47%).

Lifestyle RFs such as obesity (over 20% affected) and current smoking (16%) were also significant. Among these younger patients, 4% had a history of stroke, and peripheral vascular disease was present in 1.35%.

Cardiac interventions were common: 3% had an implantable cardioverter-defibrillator, 2% had a pacemaker, 5.5% underwent percutaneous coronary intervention, and 2.5% had prior mitral valve surgery.

Additional comorbidities included obstructive sleep apnea (18%), chronic obstructive pulmonary disease (11%), and chronic kidney disease (1.3%).

At baseline, over half of the patients under 65 were taking anticoagulants, with similar rates for aspirin and significant use of class 1 (6%) and class 3 (17%) antiarrhythmic drugs.

Mortality and hospitalization rates varied by age, with the younger cohort experiencing notably lower mortality rates compared to their older counterparts. In the under-50 age group, the 5-year and 10-year mortality rates were 5.6% and 10.3%, respectively, which approximately doubled in the 50 to 65 age group to 11.5% and 20.8%.

Hospitalization for AF, HF, and myocardial infarction was reported in 31%, 12%, and 2.7% of those under 50, while those figures increased to 38%, 19%, and 4.7% in the 50 to 65 group.

Further analysis revealed multiple cardiovascular RFs and comorbidities independently associated with all-cause mortality among those under 65. HF, peripheral vascular disease, diabetes, coronary artery disease, smoking, and obesity significantly impacted mortality rates.

Notably, chronic kidney disease and chronic obstructive pulmonary disease were also linked to poorer outcomes. Interaction analyses indicated a significant correlation between age and the impact of hypertension and HF on mortality rates.

Comparing the AF cohort with national mortality estimates highlighted a considerably higher all-cause mortality rate among the AF patients, particularly notable in younger males and females. Furthermore, adjusting for cardiac and noncardiac risk factors, AF significantly increased the mortality hazard in patients under 65 compared to a control group without AF.

This population also showed a heightened risk of hospitalization for myocardial infarction, HF, and stroke, underscoring the severe impact of AF in younger patients.

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April 24, 2024

Rising trend in atrial fibrillation risk over 20 years heightens concern for related heart and stroke complications

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In a recent Danish population-based cohort study published in the British Medical Journal, researchers analyzed the changes in lifetime risks of atrial fibrillation (AF) and complications. They compared the data between two periods, 2000-2010 and 2011-2022. They found that the lifetime risk of AF increased over the study period, and individuals with AF showed significant risks of heart failure (HF) and stroke over their lifetime.

Study: Temporal trends in lifetime risks of atrial fibrillation and its complications between 2000 and 2022: Danish, nationwide, population based cohort study. Image Credit: Magic mine / Shutterstock

Background

AF poses a growing health concern globally, with a substantial projected increase in affected populations. While improvements in mortality rates have been observed, AF remains linked to increased risks of stroke, HF, and myocardial infarction (MI). Understanding and effectively assessing AF risk, including its long-term complications, are crucial for prevention efforts. Residual lifetime risk, a measure capturing cumulative disease risk over the remaining lifespan, offers valuable insights for public health initiatives and patient education. Despite previous studies on AF lifetime risk, data on temporal trends and comprehensive complication risks are lacking. Monitoring changes in AF burden is vital for evaluating management strategies and prevention efforts, especially amid evolving stroke prevention therapies. In the present investigation involving the Danish population, researchers aimed to assess the lifetime risk of AF and its associated complications and to analyze their temporal trends spanning from 2000 to 2022.

About the study

Data were gathered from national registries, including the Danish National Patient Registry for hospital stays and outpatient contacts, the Civil Registration System for demographics and vital status, and the Danish National Prescription Registry for medication information. The study included 3,574,903 Danish individuals without AF at or after the age of 45 between 2000 and 2022. About 51.7% of the participants were women. Those aged 95 years or older were excluded. Follow-up ended at incident AF, death, age 95 years, emigration, or period end. Primary analysis used 45 years as the index age, with secondary analyses for ages 55, 65, and 75 or older. Incident AF was identified from hospital diagnoses.

A total of 362,721 individuals were followed up upon newly diagnosed AF (46.4% females). Complications, including HF, stroke, MI, or systemic embolism, were recorded post-diagnosis. Exclusions comprised pre-existing complications and events within seven days of diagnosis. The diagnosis followed strict International Classification of Diseases 10 (ICD-10) criteria with high predictive values. Analyses were conducted for index ages 45, 55, 65, and 75 years.

Study populations were characterized by assessing medical history along with family income and educational attainment. The statistical methods included the use of the Aalen-Johansen estimator for cumulative incidence, pseudo-value regression, propensity score adjustment using logistic regression, stabilized inverse propensity weighting, and subgroup analyses with interaction testing.

Results and discussion

Age distributions were found to remain consistent across the periods, while hypertension, dyslipidemia, and diabetes prevalence rose over time, whereas HF and MI prevalence reduced.

The lifetime risk of AF at the age of 45 between 2000-2022 was 27.7%, with higher risk observed among men, those with a history of certain cardiovascular conditions, and individuals with higher socioeconomic status. From 2000-2010 to 2011-2022, there was an absolute increase in lifetime risk from 24.2% to 30.9%. This trend persisted across all subgroups, with slightly higher increases among men, individuals with HF or stroke history, and those without dyslipidemia. At ages 55, 65, and 75, the lifetime risk also showed an upward trajectory, with absolute increases between the two periods.

Among individuals diagnosed with AF, HF was the most common complication, with a lifetime risk of 41.2%, followed by stroke (21.4%), MI (11.5%), and diagnosed systemic embolism (1.8%). Men generally faced higher risks of HF and MI compared to women, while women had a higher risk of stroke post-AF. History of certain cardiovascular conditions significantly increased the risk of HF post-AF. Over time, a slight decrease in the lifetime risks of stroke (-2.5%) and MI (-3.9%) was observed.

The study reports the temporal patterns in lifetime risks associated with AF and its subsequent complications for the first time. However, the study is limited by its potential underestimation of incident events due to a lack of differentiation between AF and atrial flutter and the absence of data on lifestyle factors and causes of death, among others.

Conclusion

The present Denmark-wide study reveals a concerning trend: the lifetime risk of AF has increased from one in four to one in three over the past two decades. HF emerged as the most common complication following AF, with a lifetime risk twice that of stroke. While there were slight improvements in the lifetime risks of stroke, ischemic stroke, and MI after AF, the rates remained high. These findings highlight the urgent need for effective strategies to prevent HF and stroke in patients with AF.

Journal reference:

Temporal trends in lifetime risks of atrial fibrillation and its complications between 2000 and 2022: Danish, nationwide, population-based cohort study. Vinter N. et al., British Medical Journal, 385:e077209 (2024), DOI: doi:10.1136/bmj-2023-077209, https://www.bmj.com/content/385/bmj-2023-077209

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April 22, 2024

Study shows antipsychotic drugs increase health risks in dementia patients

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In a recent British Medical Journal study, researchers assess the adverse effects associated with the use of antipsychotic drugs in people with dementia.

Study: Multiple adverse outcomes associated with antipsychotic use in people with dementia: population based matched cohort study. Image Credit: Fahroni / Shutterstock.com

The role of antipsychotics in dementia management

Individuals diagnosed with dementia undergo functional disability and progressive cognitive decline. Some common psychological and behavioral symptoms of dementia include anxiety, depression, apathy, aggression, delirium, irritability, and psychosis.

To manage psychological and behavioral symptoms of dementia, patients are commonly treated with antipsychotics. The United Kingdom National Institute for Health and Care Excellence currently recommends the use of antipsychotics only when non-drug interventions are ineffective in alleviating behavioral and psychological symptoms of dementia. However, there has been an increase in antipsychotic use during the recent coronavirus disease 2019 (COVID-19) pandemic, which has been attributed to lockdown measures and the unavailability of non-pharmaceutical treatments.

In the U.K., risperidone and haloperidol are the only antipsychotics that have received approval for the treatment of behavioral or psychological symptoms of dementia. In 2003, the United States Food and Drug Administration (FDA) highlighted the risks, such as stroke, transient ischaemic attack, and mortality, associated with the use of risperidone in older adults with dementia.

Based on multiple study reports, regulatory guidelines have been formulated in the U.K., U.S., and Europe to reduce inappropriate prescriptions of antipsychotic drugs for the treatment of behavioral and psychological symptoms of dementia. To date, few studies have provided evidence of the association between antipsychotic drug prescriptions in older adults with dementia and risks of multiple diseases, such as myocardial infarction, venous thromboembolism, ventricular arrhythmia, and acute kidney injury.

About the study

The current study investigated the risk of adverse outcomes associated with antipsychotics in a large cohort of adults with dementia. Some adverse outcomes considered in this study were venous thromboembolism, stroke, heart failure, ventricular arrhythmia, fracture, myocardial infarction, pneumonia, and acute kidney injury.

Over 98% of the U.K. population is registered with National Health Service (NHS) primary care general practice. All relevant data were collected from the electronic health records held at the Clinical Practice Research Datalink (CPRD), which is associated with over 2,000 general practices. CPRD comprises the Aurum and GOLD databases, which can be considered as broadly representative of the U.K. population.

Individuals above 50 years of age and diagnosed with dementia were recruited. Importantly, none of the study participants were under antipsychotic intervention one year before their diagnosis.

The researchers utilized a matched cohort design, in which each patient who used antipsychotics after their initial dementia diagnosis was matched using the incidence density sampling method. This method considered up to 15 randomly selected patients who were diagnosed with dementia on the same date but were not prescribed antipsychotic drugs.

Antipsychotics increase the risk of adverse effects in dementia patients

Across the two cohorts, the mean age of the participants was 82.1 years. A total of 35,339 participants were prescribed an antipsychotic during the study period.

The mean number of days between the first diagnosis of dementia and the date of a first antipsychotic prescription was 693.8 and 576.6 days for Aurum and GOLD, respectively. The most commonly prescribed antipsychotics were risperidone, haloperidol, olanzapine, and quetiapine.

The current population-based study revealed that adults with dementia prescribed antipsychotics are at a greater risk of venous thromboembolism, myocardial infarction, stroke, heart failure, pneumonia, fracture, and acute kidney injury than non-users. This observation was based on analyzing 173,910 adults with dementia selected from both databases.

The increased risk of adverse outcomes was most prevalent among current and recent users of antipsychotic drugs. After 90 days of antipsychotic use, the risk of venous thromboembolism, pneumonia, acute kidney injury, and stroke was higher than non-users. However, antipsychotic drugs did not impact the risk of ventricular arrhythmia, appendicitis, and cholecystitis.

As compared to the use of risperidone, haloperidol was significantly associated with an increased risk of pneumonia, fracture, and acute kidney injury. Although the adverse effects of haloperidol were higher than quetiapine, no significant differences were observed between risperidone and quetiapine for the risk of fracture, heart failure, and myocardial infarction. The risk of pneumonia, stroke, acute kidney injury, and venous thromboembolism was lower for quetiapine as compared to risperidone.

Conclusions

The current study highlights how antipsychotic drugs affect older adults with dementia. The use of these drugs was associated with many serious adverse outcomes, such as stroke, acute kidney injury, pneumonia, venous thromboembolism, heart failure, and myocardial infarction.

In the future, these risks must be considered, along with cerebrovascular events and mortality, while making regulatory decisions about the use of antipsychotic drugs for the treatment of dementia in older adults.

Journal reference:

Mok, L. H. P., Carr, M. J., Guthrie, B., et al. (2024) Multiple adverse outcomes associated with antipsychotic use in people with dementia: population based matched cohort study. BMJ. doi:10.1136/bmj.2023.076268

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April 19, 2024

Discovery of new vascular cell type may pave way for novel strategies to treat cardiovascular diseases

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Cardiovascular diseases, including stroke and myocardial infarction, are the world’s leading causes of mortality, accounting for over 18 million deaths a year. A team of KIT researchers has now identified a new cell type in blood vessels responsible for vascular growth. This discovery may allow for novel therapeutic strategies to treat ischemic cardiovascular diseases, i.e. diseases that are caused by reduced or absent blood flow. Nature Communications (DOI: 10.1038/s41467-024-47434-x)

In our body, a large network of blood vessels distributes blood across our organs and thereby ensures that the active cells are supplied with sufficient oxygen and nutrients to function and to maintain heart beat and brain activities for example. Occlusion of blood vessels and compromising oxygen delivery may cause neuronal or cardiac cell death culminating in stroke or heart attack. Revascularization , i. e. restoring vascular perfusion and promoting tissue regeneration, requires functional blood vessels, but how to effectively revascularize organs still is an unsolved clinical question.

Since each organ fulfills a different physiological function, vascular branching patterns differ across organs. It has long been a mystery how such unique, so-called organo-typical vascular structures develop.

From a therapeutic point of view, it is believed that understanding the organ-specific molecular control of vascular growth and patterning could open the doors for developing personalized medicine strategies to combat cardiovascular and neurodegenerative diseases and cancer.

Pioneer cells move inside the vessel walls

Scientists of the KIT led by Professor Ferdinand le Noble, Head of the Department of Cell and Developmental Biology and Director of the Zoological Institute of KIT, now discovered that one crucial element contributing to organ-dependent variability in vascular branching involves the activation of a novel vascular cell type they coined endothelial L-tip cell or pioneer cell. Pioneer cells reside inside the inner layer that lines the blood vasculature, the so-called endothelium.

Using high-end imaging techniques, the scientists found that pioneer cells move inside the vessel wall. Once they come into contact with specific signals produced by cells in the surrounding organ, pioneer cells start to make new blood vessels. To elucidate which cells produce such signals and how these signals are sensed to promote pioneer cell differentiation, the scientists used a recently developed technique called single cell sequencing.

Molecular cocktail encodes the time and place of blood vessel formation

Dr. Laetitia Preau, first author of the paper, explains: “Single cell sequencing combines detailed RNA sequencing of individual cells with bio-informatic analyses and allows precise identification of cell subtypes and the molecules these cells produce for cell-to-cell communication. Using this technique, we discovered that the vascular patterning is encoded by a distinct set of molecules that can only be sensed by a subset of endothelial cells to promote vessel growth.”

The cells in the tissue produce an organ-specific set of molecules that encode the instruction how to make a new blood vessel at that particular place and time. Once the prospective pioneer cell senses and unravels this specific tissue-derived molecular code, it will initiate the vascular growth process.

Foundations for new therapeutic approaches

It turned out that several organ-specific vascular growth code molecules are drug-targetable, i.e. react to externally added chemicals.

To explore the therapeutic avenues, we are collaborating with chemists, tissue engineers, and artificial intelligence (AI) specialists at the 3ROCKIT platform of the Health Technologies Center established recently at Karlsruhe Institute of Technology (KITHealthTech). We hope to identify novel smart molecules to target the vascular growth process that may benefit patients suffering from ischemic cardiovascular diseases, such myocardial infarction and stroke, as well as from certain forms of cancer.”

Professor Ferdinand le Noble

The study was financed by the German Research Foundation (DFG) and carried out by KIT in cooperation with the German Center for Cardiovascular Research (DZHK) at its partners sites in Heidelberg and Munich and the Max Planck Institute for Molecular Biomedicine in Münster.

Source:

Karlsruhe Institute of Technology

Journal reference:

Préau, L., et al. (2024). Parenchymal cues define Vegfa-driven venous angiogenesis by activating a sprouting competent venous endothelial subtype. Nature Communications. doi.org/10.1038/s41467-024-47434-x.

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April 18, 2024

Bidirectional Mendelian randomization uncovers link between plasma metabolites and heart attack risk

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Myocardial infarction, more commonly known as a heart attack, is a leading cause of death worldwide. Biomarkers called plasma metabolites may play a key role in the physiological pathways involved in myocardial infarctions. Recently published research used a methodological approach called bidirectional Mendelian randomization to understand more about these biomarkers and what they can tell doctors about heart attack risk.

The research was published in the Journal of Geriatric Cardiology on February 28.

Bidirectional Mendelian randomization studies represent a robust methodological approach, with numerous advantages not commonly present in traditional research methodologies. These include mitigating the impact of confounding factors on conclusions and exploring reverse causation, thereby providing a more reliable foundation for casual inferences. This study employed a bidirectional Mendelian randomization approach to investigate the relationship between plasma metabolites and myocardial infarction, offering new insights into the early diagnosis and potential treatment of myocardial infarction.”

Qiang Wu from the Senior Department of Cardiology, the Sixth Medical Center, Chinese PLA General Hospital, Beijing, China

By using data sets from large-scale genome-wide association studies, researchers were able to cast a wide net to try and understand more about the role plasma metabolites play in myocardial infarction. The data source included 461,823 individuals of European descent. Of those, 20,917 individuals had myocardial infarction and 440,906 individuals did not. A total of 24,172,914 single nucleotide polymorphisms were identified in that data set to be associated with myocardial infarction. Bidirectional Mendelian randomization narrows down this large amount of data and determines the relationship between plasma metabolites and myocardial infarction.

This analysis uncovered 198 unique plasma metabolites that were identified to have a significant association with myocardial infarction, of which 14 plasma metabolites had a direct relationship with myocardial infarction risk. “We identified 14 plasma metabolites associated with myocardial infarction, of which 8 plasma metabolites were linked to a decreased risk and 6 plasma metabolites were linked to an increased risk, underscoring the complicated nature of metabolic pathways influencing heart attack risk,” said Dong-Hua LI from Department of Cardiovascular Medicine, Minzu Hospital of Guangxi Zhuang Autonomous Region, Guangxi, China. “The robustness of our findings was strengthened by the application of bidirectional Mendelian randomization, enabling a thorough exploration of causality.”

Of the 14 plasma metabolite biomarkers identified in this study, 13 plasma metabolite biomarkers had never been identified as potential biomarkers associated with myocardial infarction before. These biomarkers offer a new option for developing diagnostic tests, routine screenings, and treatments for heart attack.

Looking to next steps, researchers are hoping to learn more about the mechanisms of these plasma metabolites and how they are related to myocardial infarction. For example, there were 8 plasma metabolites that were associated with a decreased risk of myocardial infarction and researchers speculate that anti-inflammatory properties associated with metabolites are at play, reducing oxidative stress in the body. However, additional research is needed to confirm this hypothesis.

“Timely detection using metabolic signatures could usher in a new era of preventive cardiology, where interventions are tailored to an individual’s metabolic profile. Furthermore, understanding the metabolic underpinnings of myocardial infarction will contribute to the development of point-of-care diagnostic tools, providing rapid and accessible assessments. Thus, the findings of the study can revolutionize clinical practice by enabling early and precise diagnoses, ultimately causing more effective and tailored treatment strategies,” said Qiang SU from Department of Cardiology, Jiangbin Hospital of Guangxi Zhuang Autonomous Region, Guangxi, China.

Other contributors include Jing-Sheng LAN, You-Yi HUANG, Lan-Jin WU, Zhi-Qing QIN, and Ying HUANG from Minzu Hospital of Guangxi Zhuang Autonomous Region in Guangxi, China; Shuo CHEN and Xin HAO from Chinese PLA General Hospital in Beijing, China; and Wan-Zhong HUANG, Ting ZENG, and Hua-Bin SU from Jiangbin Hospital of Guangxi Zhuang Autonomous Region in Guangxi, China.

The Guangxi Natural Science Foundation, the Key Research and Development Program of Guangxi, and the Chongzuo Science and Technology Bureau Planning Project funded this research.

Source:

Tsinghua University Press

Journal reference:

Li, D.-H., et al. (2024). Plasma metabolites and risk of myocardial infarction: a bidirectional Mendelian randomization study. Journal of Geriatric Cardiology. doi.org/10.26599/1671-5411.2024.02.002.

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April 17, 2024

Beta-blockers show no benefit for heart attack patients with normal heart function

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In a recent study published in The New England Journal of Medicine, researchers conducted the Randomized Evaluation of Decreased Usage of Beta-Blockers after Acute Myocardial Infarction (REDUCE-AMI) trial to determine whether long-term oral beta-blocker therapy could reduce the risk of any cause or incident MI-related mortality among individuals with acute myocardial infarction but preserved left ventricular ejection fraction compared to no beta-blocker treatment.

Study: Beta-Blockers after Myocardial Infarction and Preserved Ejection Fraction. Image Credit: aipicte / Shutterstock

Background

Beta-blockers are beneficial in treating heart failure patients and those with reducing ejection fractions; however, these findings are from 1980s trials of patients with massive myocardial infarctions and systolic dysfunction in the left ventricle. Meta-analytical research indicated that beta-blockers do not appear to lower mortality in contemporary reperfusion techniques.

There is a lack of data from recent randomized clinical studies on the efficacy of long-term use of beta-blockers among acute myocardial infarction patients with intact ejection fraction. Previous Cochrane reviews underscore the need for novel research studies in this target population. Despite the absence of convincing scientific evidence of medication benefit, current recommendations strongly advocate beta-blocker therapy following a myocardial infarction.

About the study

In the present open-label, prospective, parallel-group trial, researchers evaluated the impact of beta-blocker therapy on reducing mortality among acute MI patients.

The team conducted the registry-based trial between September 2017 and May 2023 at 45 sites across New Zealand, Sweden, and Estonia. They randomized participants with prior acute MI who underwent coronary angiographies and had ≥50% ejection fraction from the left ventricle to receive 1:1 long-term therapy with beta-blockers such as ≥100 mg/day of metoprolol or ≥5 mg/day of bisoprolol (intervention group) or no such therapy.

All participants had obstructive coronary heart disease, as determined from coronary angiographies (i.e., ≥50% stenosis, ≤0.8 fractional flow reserves, or ≤0.9 instant wave-free segment ratios) before randomization. The primary outcome was the composite measure of all-cause or incident MI-related mortality. Secondary outcomes included cardiovascular disease-related mortality and hospital admission for atrial fibrillations or heart failure.

Safety outcomes included hospital admission for hypotension, second and third-degree atrioventricular blocks, bradycardia, syncope, or pacemaker implantation, and hospital admission due to chronic obstructive pulmonary disease (COPD), asthma, or stroke. Other endpoints included dyspnea [diagnosed using the New York Heart Association (NYHA) recommendations] and angina pectoris (diagnosed using the Canadian Cardiovascular Society guidelines) six to 10.0 weeks or 11.0 to 13.0 months after treatment. The team used Cox proportional-hazards regressions to determine the hazard ratios (HR) for analysis. They performed sensitivity analyses, adjusting for age, country, diabetes, and prior myocardial infarction. The Swedish population registry provided data on death or emigration, and the Swedish Web System for Enhancement and Development of Evidence-based Care in Heart Disease Evaluated According to Recommended Therapies (SWEDEHEART) register collected data on incident myocardial infarctions. The national cause-of-death registry provided cardiovascular-related mortality data, while the national patient registry provided data on atrial fibrillation, heart failure, and safety outcomes.

Results

The researchers enrolled 5,020 MI patients (95% from Sweden) who followed up for a median of 3.50 years until November 16, 2023. The median participant age was 65.0 years, 23% were female, and 35% had myocardial infarction with an elevation in the ST segment. Among the participants, 46% were hypertensive, 14% were diabetic, and 7.1% had a prior myocardial infarction. Of 2,508 beta-blocker recipients, 1,560 (62%) and 948 (38%) received metoprolol and bisoprolol, respectively.

Coronary angiography showed one-vessel involvement among 55% of MI patients, two vessels involved among 27%, and three vessels involved among 17% of patients. The team performed percutaneous coronary interventions in 96% of patients, with coronary artery bypass grafting (CABG) among 3.9%. At hospital discharge, 97% received aspirin, P2Y12 receptor blockers, angiotensin-converting enzyme (ACE) inhibitors, and statins.

The researchers observed the primary endpoint among 7.9% (199 out of 2,508) of beta-blocker recipients and 8.3% (208 out of 2,512) of non-recipients (HR, 0.96). Beta-blockers did not lower the cumulative incidence rates of secondary endpoints (all-cause mortality, 3.90% and 4.10% among beta-blocker recipients and non-recipients, respectively); cardiovascular disease-related mortality, 1.50% and 1.30%, respectively; myocardial infarctions, 4.50% and 4.70%; hospital admission due to atrial fibrillations, 1.10% and 1.40%; and hospital admission due to heart failures, 0.80% and 0.90%).

Concerning safety endpoints, the researchers observed hospital admission due to atrioventricular blocks, bradycardia, syncope, hypotension, or pacemaker implantation among 3.40% of beta-blocker recipients and 3.20% of non-recipients; hospital admission due to COPD or asthma in 0.60% and 0.60%, respectively, and hospital admission due to stroke among 1.40% and 1.80% of beta-blocker recipients and non-recipients, respectively. Subgroup analyses yielded similar results.

Overall, the study findings showed that long-term use of beta-blockers did not reduce the risk of all-cause or incident myocardial infarction-related mortality in patients with an acute MI who underwent coronary angiography but retained ≥50% ejection fraction from the left ventricle compared to no treatment with beta-blockers.

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April 9, 2024

Empagliflozin shows mixed results in heart attack patients

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Use of the sodium glucose cotransporter-2 (SGLT-2) inhibitor empagliflozin following a heart attack did not show a significant benefit in reducing overall heart failure hospitalizations or death from any cause, according to a study presented at the American College of Cardiology’s Annual Scientific Session. However, researchers said the drug may be helpful in reducing heart failure risks, including hospitalization, following a heart attack.

Despite falling short of its primary endpoint, results from the EMPACT-MI trial found that people who took empagliflozin had a significantly lower risk of certain outcomes directly related to heart failure, including first hospitalization for heart failure, total hospitalization for heart failure and a composite of heart failure hospitalization and death from heart failure, without any increased risk of adverse events.

We found that empagliflozin did not reduce mortality after a heart attack but did reduce the risk of heart failure after heart attack. To have a 25% to 30% reduction in heart failure hospitalizations is pretty clinically meaningful, but if you put it together with all-cause mortality, it was not a positive study for our primary endpoint.”

Javed Butler, MD, president of the Baylor Scott and White Research Institute in Dallas, distinguished professor of medicine at the University of Mississippi in Jackson, Mississippi, and study’s lead author

SGLT-2 inhibitors were initially approved to treat Type 2 diabetes by lowering blood sugar. As evidence has mounted pointing to their benefits in reducing heart failure and other forms of heart disease, researchers have sought to determine whether these drugs could help to prevent heart failure even in people without diabetes or chronic kidney disease.

A heart attack can damage the heart muscle in ways that sometimes lead to heart failure, a condition in which the heart becomes too weak or too stiff to effectively pump blood throughout the body. The EMPACT-MI trial was designed to determine whether SGLT-2 inhibitors could safely help to prevent heart failure and reduce mortality in people with a high risk of heart failure following a heart attack.

The study enrolled 6,522 people treated for acute myocardial infarction at 451 centers in 22 countries. Participants had no history of heart failure but had at least one heart failure risk factor in addition to signs of potential heart dysfunction as indicated by a newly lowered left ventricle ejection fraction to below 45% and/or signs or symptoms of congestion requiring treatment. About 32% had Type 2 diabetes. On average, participants were 64 years old and approximately 25% were women and 84% were White.

Within 14 days of being admitted to the hospital for a heart attack, half of the participants were randomly assigned to receive empagliflozin at a dose of 10 mg daily, while the other half received a placebo. Researchers tracked outcomes for a median of just under 18 months.

The study’s primary composite endpoint occurred in 8.2% of those who received empagliflozin and 9.1% of those receiving a placebo, a difference that was not statistically significant. There was also no difference in the rate of death from any cause, which occurred in 5.2% of those receiving empagliflozin and 5.5% of the control group.

All secondary endpoints related specifically to heart failure outcomes were significantly reduced among patients who received empagliflozin. For example, those receiving empagliflozin were 23% less likely to experience a first heart failure hospitalization and 33% less likely to experience any heart failure hospitalization—including recurrent hospitalizations—compared with those taking a placebo. The composite rate of total heart failure hospitalizations and death from heart failure was also 31% lower among those receiving empagliflozin.

Among patients who were not taking common heart failure therapies such as diuretics, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor/neprilysin inhibitor (ARNI) at the time of their initial hospital discharge, those taking empagliflozin were significantly less likely to start such therapies within six months compared with those taking a placebo.

“In terms of heart failure outcomes, the data is not only strong, but it’s consistent with what we’ve found over the past 10 years in yet another population,” Butler said. “This finding is completely consistent in both direction and magnitude with other studies of SGLT-2 inhibitors in populations with diabetes and chronic kidney disease.”

While as a pragmatic trial design to simplify trial procedures and make it easier on both the participants and the sites, the study had limitations that may have influenced the findings, researchers said. For example, because outcomes were not adjudicated by independent reviewers, outpatient heart failure events were not formally captured as part of the primary endpoint. However, researchers said data on outpatient heart failure visits were collected as part of the study protocols for assessing adverse events. An analysis of these events showed outpatient visits for heart failure were substantially lower in participants who received empagliflozin compared with placebo.

Another limitation was the use of all-cause mortality as part of the primary endpoint, which meant that deaths unrelated to heart failure were included in the endpoint even though the study drug was unlikely to influence them. There were also some unusual circumstances that may have influenced rates of both hospitalization and death, including the COVID-19 pandemic and conflicts involving Russia, Ukraine and Israel, all countries that participated in the trial.

Finally, researchers said that the follow-up period may have been too short to fully capture any difference in mortality related to heart failure. Since people who developed heart failure following their heart attack typically did not begin to show heart failure symptoms until a few months later, any reductions in mortality would not be expected to emerge until after that.

“We just did not have long enough follow-up to see whether that heart failure prevention would lead to a benefit in mortality, but it’s a reasonable clinical thing to say that if you’re preventing heart failure, it’s a good thing,” Butler said.

The study was funded by Boehringer Ingelheim and Eli Lilly.

This study was simultaneously published online in the New England Journal of Medicine at the time of presentation.

Butler will be available to the media in a press conference on Saturday, April 6, 2024, at 10:45 a.m. ET / 14:45 UTC in Room B203.

Butler will present the study, “Empagliflozin After Acute Myocardial Infarction: Results of the EMPACT-MI Trial,” on Saturday, April 6, 2024, at 9:30 a.m. ET / 13:30 UTC in the Hall B-1 Main Tent.

Source:

American College of Cardiology

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April 8, 2024

More women experience cardiovascular disease following a depression diagnosis than men

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People with depression face an increased risk of cardiovascular disease (CVD); however, more women experience CVD following a depression diagnosis than men, according to a new study published today in JACC: Asia. The study investigates the connection between depression and CVD, shedding light on potential mechanisms that contribute to its sex-based differences and underscoring the importance of tailoring CVD prevention and management strategies according to sex-specific factors.

Depression is the third leading cause of morbidity worldwide. Prior research shows that it is associated with a heightened risk of cardiovascular events, including myocardial infarction (MI), angina, stroke and CV mortality. Women with depression are at greater relative risk of developing heart-related negative health outcomes than men, but there is still controversy over the evidence on sex differences in the impact of depression on heart health and the mechanisms underlying this are not well understood.

The identification of sex-specific factors in the adverse effects of depression on cardiovascular outcomes may help in the development of targeted prevention and treatment strategies that address the specific CVD risks faced by depressed patients. A better understanding will allow healthcare providers to optimize care for both men and women with depression, leading to improved CVD outcomes for these populations.”

Hidehiro Kaneko, MD, assistant professor at the University of Tokyo in Japan and a corresponding author of the study

Researchers in this study evaluated the association between depression and subsequent CVD events by conducting an observational cohort study using the JMDC Claims Database between 2005 and 2022. They identified 4,125,720 participants who met the study’s criteria. The median age was 44 (36-52) years, and 2,370,986 participants were men. Depression was defined as those clinically diagnosed before their initial health checkup.

Using standardized protocols, the study collected participant’s body mass index (BMI), blood pressure and fasting laboratory values at their initial health checkup. The primary outcome was a composite endpoint including MI, angina pectoris, stroke, heart failure (HF) and atrial fibrillation (AF).

Researchers analyzed the statistical significance of differences in clinical characteristics between participants with and without depression. Results indicate that the hazard ratio of depression for CVD was 1.39 in men and 1.64 in women compared with participants without depression. Models also indicate that hazard ratios of depression for MI, angina pectoris, stroke, HF, and AF were higher for women than for men.

Study authors highlight an important discussion regarding the potential mechanisms that may contribute to why depression impacts women’s heart health more than men’s. One explanation is that women may experience more severe and persistent symptoms of depression compared to men, and they may be more likely to have depression during critical periods of hormonal changes, such as pregnancy or menopause.

Other mechanisms include women’s greater susceptibility to traditional risk factors when depressed, such as hypertension, diabetes and obesity, which may contribute to the development of CVD. Differences in healthcare utilization and treatment between men and women and sex-specific differences in biological factors, such as genetics and hormonal profiles, may also increase women’s CVD risk.

“Our study found that the impact of sex differences on the association between depression and cardiovascular outcomes was consistent,” Kaneko said. “Healthcare professionals must recognize the important role of depression in the development of CVD and emphasize the importance of a comprehensive, patient-centered approach to its prevention and management. Assessing the risk of CVD in depressed patients and treating and preventing depression may lead to a decrease of CVD cases.”

Limitations of the study include the inability to establish direct causality between depression and cardiovascular events and the inability to accurately reflect the severity or duration of depressive symptoms. Potential confounding factors that may influence the association between depression and CVD were not accounted for, such as socioeconomic status. Researchers also acknowledge that COVID-19 may have been a confounder.

Source:

American College of Cardiology

Journal reference:

Senoo, K., et al. (2024) Sex Differences in the Association Between Depression and Incident Cardiovascular Disease. JACC: Asia. doi.org/10.1016/j.jacasi.2023.11.015.

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March 12, 2024

Tag: Myocardial Infarction

Background

Study design

Important observations

Study significance

Background

About the study

Study results

Background

About the study

Results and discussion

Conclusion

The role of antipsychotics in dementia management

About the study

Antipsychotics increase the risk of adverse effects in dementia patients

Conclusions

Pioneer cells move inside the vessel walls

Molecular cocktail encodes the time and place of blood vessel formation

Foundations for new therapeutic approaches

Background

About the study

Results