Think Vitamin Supplements Improve Your Heart Health? Think Again!

MedicalResearch.com Interview with:
“Pills Vitamins Macro April 22, 2012 4” by Steven Depolo is licensed under CC BY 2.0David J.A. Jenkins, MD, PhD, DSc
Professor and Canada Research Chair in Nutrition and Metabolism
Department of Nutritional Sciences
University of Toronto 

MedicalResearch.com: What is the background for this study?

Response: The study was requested by the editor of JACC (Dr. Valentin Fuster) due to the widespread use of vitamin and mineral supplementation by the public and the requirement to know if there were any benefits or harms for cardiovascular disease.

Our study was a follow-up to the US Preventive Services Task Force 2013 recommendations.

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More Protein Associated With Moderate Increase in Heart Failure in Men (except for fish and eggs)

MedicalResearch.com Interview with:
“mmmm Meat” by Glen MacLarty is licensed under CC BY 2.0
Jyrki Virtanen, PhD
Adjunct professor of nutritional epidemiology
Heli Virtanen, MSc

University of Eastern Finland
Institute of Public Health and Clinical Nutrition
Kuopio, Finland 


MedicalResearch.com: What is the background for this study? What are the main findings?

Response: Previous studies have found that animal sources of protein may have an adverse impact on the risk of cardiovascular diseases, like myocardial infarct, whereas plant sources of protein have had an opposite impact.

In this study we investigated that how protein intake from different dietary sources is associated with developing heart failure in men during the study’s follow-up. During the mean follow-up time of about 22 years, 334 men developed heart failure.

The main finding of the study was that higher protein intake was associated with a moderately higher risk of heart failure and the findings were similar with protein from most dietary sources, although the association was stronger with protein from animal sources. Only protein from fish and eggs were not associated with the risk in our study. Continue reading

Study Finds Plant-Based Diet Can Reduce Cardiovascular Death by 40%

MedicalResearch.com Interview with:
“Vegetarian Skewers” by Geoff Peters is licensed under CC BY 2.0Hana Kahleova, M.D., Ph.D.
Director of clinical research
Physicians Committee for Responsible Medicine
Washington, DC 20016 

MedicalResearch.com: What is the background for this study? What are the main findings? 

Response: In this study, my research team and I reviewed multiple clinical trials and observational studies to determine the links between diet and cardiovascular disease (CVD) risk. We found that a healthy diet can reduce the risk of heart attack by more than 80 percent—something no drug has ever accomplished.

We also found strong and consistent evidence that plant-based dietary patterns (with few or no animal products and rich in fruits, vegetables, grains, and legumes) can prevent and even reverse atherosclerosis and decrease other markers of CVD risk, including blood pressure, cholesterol, and weight. We found that a plant-based diet can reduce the risk of death from cardiovascular disease by about 40 percent overall.  Continue reading

PlaqueTec Liquid Biopsies Give Alternative Data To Systemic Biomarkers

MedicalResearch.com Interview with:
PlaqueTec liquid biopsiesDr. Nick West, MD
PlaqueTec Chief Medical Officer and Consultant Interventional Cardiologist
Royal Papworth Hospital NHS Foundation Trust  

MedicalResearch.com: What is the background for this study?

Response: Recent data have identified residual inflammatory risk as a potential therapeutic target to modulate future risk of coronary and vascular events independent of cholesterol lowering1. This approach has now been validated by the CANTOS study, showing reduction of peripheral blood levels of high-sensitivity CRP (hsCRP) and consequent reduction of the occurrence of major cardiac events in patients who had sustained a myocardial infarction2,3. Although controversy continues to rage regarding the relevance of ‘vulnerable plaque’ versus ‘vulnerable patient’ in the causation of acute coronary events, evolving data suggest a complex interplay between a proinflammatory milieu and ‘vulnerable’ plaque phenotypes 4,5 .

We used a novel dedicated intracoronary sampling catheter, the PlaqueTec Liquid Biopsy SystemTM (LBS), and sought to correlate systemic inflammatory indices with degree of local coronary inflammatory activity. The LBS has previously been validated to safely delineate the presence of gradients of inflammatory biomolecules in human coronary artery disease6. We measured blood levels of a large panel of inflammatory biomolecules using multiplexed assays in peripheral blood and in coronary-derived blood samples after balloon dilatation of coronary stenoses during coronary angioplasty, and assessed systemic levels of hsCRP by ELISA.

MedicalResearch.com: What are the main findings? 

Response: Statistical analysis using K-means indicated our patient population (n=23), predominantly patients with stable angina, segregated into 2 discrete clusters of high and low overall coronary inflammatory states. However, when compared with peripheral (systemic) levels of the same inflammatory biomolecules in each cluster, there was no meaningful relationship. Additionally, there was no difference between median hsCRP measurements between the 2 clusters. Taken together, these data suggest that simply measuring peripheral markers of inflammation may not be able to determine local inflammatory activity within the coronary artery itself. 

MedicalResearch.com: What should readers take away from your report?
What recommendations do you have for future research as a result of this work?

Response: These data provide interesting and hypothesis-generating data that explore the mechanisms of benefit in vascular risk by reducing systemic inflammation; rather than hsCRP acting as a simple ‘barometer’ for likelihood of events, it appears that presence of coronary inflammation may be an independent entity. Further studies are needed to address the complex relationship between systemic and coronary inflammation, and their respective interaction with ‘vulnerable’ plaque phenotypes in modulating patient events.

Disclosures: Dr West acts as a consultant to, and holds equity in, PlaqueTec Ltd.

Citations:

  1. Ridker PM. Residual inflammatory risk: addressing the obverse side of the atherosclerosis prevention coin. Eur Heart J 2016; 37: 1720-22.
  2. Ridker PM, Everett BM, Thuren T et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease. N Engl J Med 2017; 377: 1119-31.
  3. Ridker PM, MacFadyen JG, Everett BM et al. Relationship of C-reactive protein reduction to cardiovascular event reduction following treatment with canakinumab: a secondary analysis from the CANTOS randomissed controlled trial. Lancet 2018; 391: 319-28.
  4. Libby P, Pasterkamp G. Requiem for the vulnerable plaque. Eur Heart J 2015; 36: 2984-7.
  5. Hansson GK, Libby P, Tabas I. Inflammation and plaque vulnerability. J Intern Med 2015; 278: 483-93.
  6. West NEJ, Corrigan JP, Owen RHG et al. Percutaneous sampling of local biomolecule gradients across coronary artery atherosclerotic plaques. J Am Coll Cardiol Basic Trans Science 2017; 2: 646-54.

Citation:

PlaqueTec Data Presented at EAS Show Lack of Correlation 
between Localised Coronary Artery Inflammatory Biomarker Expression and Systemic Elevation of Biomarkers including hsCRP

 

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Reduced Heart Rate Variability May Be Biomarker of Depression Risk

MedicalResearch.com Interview with:

Viola Vaccarino, MD, PhD Department of Epidemiology and Division of Cardiology Professor, Department of Medicine Emory University School of Medicine Atlanta, Georgia

Dr. Vaccarino

Viola Vaccarino, MD, PhD
Department of Epidemiology and Division of Cardiology
Professor, Department of Medicine
Emory University School of Medicine
Atlanta, Georgia 

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: Previous studies have shown that people with depression tend to have lower heart rate variability (HRV), an index of autonomic nervous system dysregulation derived by monitoring the electrocardiogram over time, usually for 24 hours. Other literature, however, has pointed out that autonomic dysregulation (as indexed by reduced HRV) may also cause depression. Thus, the direction of the association between reduced HRV and depression still remains unclear. In addition, these two characteristics could share common pathophysiology, making shared familial background and genetic factors potential determinants of this association.
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Amyloid Biomarker Predictive of Mortality in Non-STEMI Heart Attack

MedicalResearch.com Interview with:

Prof. Dr. med. Konstantinos Stellos,MD, FAHA, FESC Cardiovascular Research Centre, Institute of Genetic Medicine Newcastle upon Tyne United Kingdom

Prof. Stellos

Prof. Dr. med. Konstantinos Stellos,MD, FAHA, FESC
Cardiovascular Research Centre, Institute of Genetic Medicine
Newcastle upon Tyne
United Kingdom

MedicalResearch.com: What is the background for this study?

 

Response: Risk stratification of patients with a non-ST-segment elevation acute coronary syndrome (NSTE-ACS) remains a major challenge in clinical cardiology. Risk stratification is important to identify patients at high risk, to whom an early coronary intervention with optimal adjunctive medical therapy shall be applied to reduce that risk. Conversely, it is equally important to identify patients at low risk, to whom a potentially hazardous invasive therapy or a multi-drug administration shall be avoided. Current ACC/AHA and ESC guidelines agree in a standardized approach that uses Global Registry of Acute Coronary Events (GRACE) score, a well validated scoring system, to calculate a patient’s risk and guide triage and management decisions.

Amyloid-β (Aβ) 1-40 and 1-42 peptides (Aβ40 and Aβ42), are proteolytic fragments of a larger protein, the amyloid precursor protein (APP) cleaved by β- and γ-secretases, found in typical brain amyloid deposits in Alzheimer’s disease. Many lines of evidence support a role of Aβ40 in cardiovascular disease as a peptide with pro-inflammatory and pro-thrombotic properties. Most cardiovascular risk factors seem to affect APP metabolism and thus, Aβ production and its soluble circulating APP770 isoform are elevated in patients with ACS_ENREF_15, suggesting a role for Aβ40 in the triggering and outcome of ACS in stable CAD patients. Although vascular inflammation is considered as a hallmark in the pathophysiologic pathways of coronary artery disease (CAD) and novel mechanisms are continuously recognized in its pathogenesis, no inflammatory marker is currently recommended for risk stratification of patients with NSTE-ACS individually or as a component of the GRACE score. This may partly explain the moderate discriminative ability of GRACE score in some studies, especially in older patients and those after early percutaneous coronary intervention (PCI).

In this retrospective study, we used data from two independent prospective cohorts, the Heidelberg study (n=1,145) and the validation multicenter international APACE (Advantageous Predictors of Acute Coronary Syndrome Evaluation, n=734) study and determined the clinical prognostic and reclassification value of baseline circulating Aβ40 levels in the prediction of mortality over the GRACE risk score in patients with NSTE-ACS across a median follow-up of 21.9 ( Heidelberg cohort) and 24.9 months (APACE cohort), respectively.

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Oral Anticoagulants Still Underused in AFib Patients

MedicalResearch.com Interview with:
Anna Gundlund, MD, PhD

Herlev-Gentofte Hospital, Department of Cardiology
Denmark 

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: Atrial fibrillation increases a person’s risk of ischemic strokes up to 5-fold. Oral anticoagulation therapy lowers this risk effectively (>60%) and is therefore recommended for patients with atrial fibrillation and at least 1-2 other risk factors for stroke.

Our study show, that oral anticoagulation therapy is still underused in patients with atrial fibrillation – even after a stroke event. In stroke survivors with atrial fibrillation, oral anticoagulation therapy were associated with better outcomes than no oral anticoagulation therapy.  Continue reading

Genetic Factors Control Heart Rate in Response to Exercise

MedicalResearch.com Interview with:

Professor Patricia Munroe PhD Professor of Molecular Medicine William Harvey Research Institute Barts and The London School of Medicine and Dentistry Queen Mary University of London

Prof. Munroe

Prof. Patricia Munroe PhD
Professor of Molecular Medicine
William Harvey Research Institute
Barts and The London School of Medicine and Dentistry
Queen Mary University of London

MedicalResearch.com: What is the background for this study?

Response: Over the years, it has become increasingly evident that impaired capacity to increase heart rate during exercise and reduce heart rate following exercise are important predictors of all-cause and cardiovascular mortality. A person’s capability to regulate their heart rate is the result of complex interactions of biological systems, including the autonomic nervous and hormonal systems. Prior work has demonstrated that genetic factors significantly contribute to variations in resting heart rate among different individuals, but less was known about the genetic factors modulating the response of heart rate to exercise and recovery.

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LPA Gene Variants Linked To Cardiac Events Despite Statins

MedicalResearch.com Interview with:

Wei-Qi Wei, MD, PhD Assistant Professor Department of Biomedical Informatics Vanderbilt University Nashville, TN 37203

Dr. Wei-Qi Wei

Wei-Qi Wei, MD, PhD
Assistant Professor
Department of Biomedical Informatics
Vanderbilt University
Nashville, TN 37203

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: The study was motived by the clinical observation that some patients develop coronary heart disease events despite taking statins, one of our most effective drugs to reduce cardiovascular risk. We collected data within the eMERGE network of people taking statins and monitored them for development of coronary heart disease events over time.  We  conducted a genome-wide association study of those with events compared to those without events.

Our results showed that single nucleotide polymorphisms (SNPs) on the LPA gene were associated with a significantly increased risk of coronary heart disease events. Individuals with the variant were 50% more likely to have an event. More importantly, even among patients who achieved ideal on-treatment LDL cholesterol levels (<70 mg/dL), the association remained statistically significant.

We then did a phenome-wide association study to see if other diseases or conditions were associated with these LPAvariants. The major associated conditions were all cardiovascular. This sort of study can highlight potential other indications for a drug targeting this pathway and suggest potential adverse events that might be experienced from targeting this pathway. Clearly, more and larger studies will be needed to truly understand the potential risks and benefits of a future drug targeting this pathway.  Continue reading

Silent MI Before Acute Heart Attack Can Be Poor Prognostic Indicator

MedicalResearch.com Interview with:

Robin Nijveldt  MD PhD FESC Radboudumc Department of Cardiology The Netherlands

Dr. Nijveldt

Robin Nijveldt  MD PhD FESC
Radboudumc, Department of Cardiology and
VU University Medical Center
Department of cardiology
the Netherlands

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: We know from previous studies that patients with unrecognized myocardial infarcts have worse prognosis than people without infarcts.

It was currently unknown in how many patients presenting with a first acute myocardial infarction had previous unrecognized MI, and if so, if this is still a prognostic marker on long term follow-up.

In this paper we studied 405 patients from 2 academic hospitals in the Netherlands, with an average follow-up duration of 6.8 years. We found that silent MI was present in 8.2% of patients presenting with first acute MI, and that silent MI is a strong and independent predictor for adverse long-term clinical outcome such as death (HR 3.69) or the composite end point of death, reinfarction, ischemic stroke, or CABG (HR 3.05). Additionally, it appears that ECG is of limited value to detect silent MI, since our study did not reveal an association with long-term clinical outcome.

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