Heart Procedures and Risk

O AMICOR Flávio Kanter chamou atenção: Big Study Finds Many Heart Procedures Won’t Cut Risk of Having Heart Attack

Coronary artery disease

Estimated costs of hospitalization due to coronary artery disease attributable to familial hypercholesterolemia in the Brazilian public health system

• May 2018

• DOI: 
• 10.20945/2359-3997000000030

• License
• CC BY 4.0

• Luciana R Bahia
• Roger dos Santos Rosa
• Raul D. Santos
• Denizar Vianna Araujo

Abstract

Objective: Cardiovascular diseases are the leading cause of death in Brazil, imposing substantial economic burden on the health care system. Familial hypercholesterolemia (FH) is known to greatly increase the risk of premature coronary artery disease (CAD). This study aimed to estimate the economic impact of hospitalizations due to CAD attributable to FH in the Brazilian Unified Health Care System (SUS). Subjects and methods: Retrospective, cross-sectional study of data obtained from the Hospital Information System of the SUS (SIHSUS). We selected all adults (≥ 20 years of age) hospitalized from 2012--2014 with primary diagnoses related to CAD (ICD-10 I20 to I25). Attributable risk methodology estimated the contribution of FH in the outcomes of interest, using international data for prevalence (0.4% and 0.73%) and relative risk for events (RR = 8.56). Results: Assuming an international prevalence of FH of 0.4% and 0.73%, of the 245,981 CAD admissions/year in Brazil, approximately 7,249 and 12,915, respectively, would be attributable to an underlying diagnosis --of FH. The total cost due to CAD per year, considering both sexes and all adults, was R$ 985,919,064, of which R$ 29,053,500 and R$ 51,764,175, respectively, were estimated to be attributable to FH. The average cost per FH-related CAD event was R$ 4,008. Conclusion: Based on estimated costs of hospitalization for CAD, we estimated that 2.9-5.3% are directed to FH patients. FH can require early specific…

Oral Anticoagulation : Atrial Fibrillation & Percutaneous Coronary Intervention

Journal Club: Clinical Updates in Oral Anticoagulation for Patients With Atrial Fibrillation Requiring Percutaneous Coronary Intervention

Evaluating Treatment Strategies With a Non–Vitamin K Oral Anticoagulant in Patients With Atrial Fibrillation Undergoing Percutaneous Coronary Intervention

Part 1 of 2 from "Journal Club: Clinical Updates in Oral Anticoagulation for Patients With Atrial Fibrillation Requiring Percutaneous Coronary Intervention"

Based on a review of "Prevention of Bleeding in Patients with Atrial Fibrillation Undergoing PCI" (The New England Journal of Medicine. 2016;375:2423-2434).

Content developed in concert with the faculty.
Release Date: 30 January 2017
Expiration Date: 29 July 2018

Learning Objectives

• Review guidelines and data on the use of oral anticoagulation in patients with atrial fibrillation (AF) requiring percutaneous coronary intervention (PCI)
• Summarise recently published data from a study evaluating a non–vitamin K oral anticoagulant (NOAC) for the treatment of patients with AF requiring PCI
• Discuss how these data will impact clinical practice

BAG3

BAG3 protein plays critical role in protecting heart from reperfusion injury, Temple research shows

November 17, 2016

(Philadelphia, PA) – The inability of cells to eliminate damaged proteins and organelles following the blockage of a coronary artery and its subsequent re-opening with angioplasty or medications – a sequence known as ischemia/reperfusion – often results in irreparable damage to the heart muscle. To date, attempts to prevent this damage in humans have been unsuccessful. According to a new study by scientists at the Lewis Katz School of Medicine at Temple University (LKSOM), however, it may be possible to substantially limit reperfusion injury by increasing the expression of a protein known as Bcl-2-associated athanogene 3 (BAG3)./.../

CVD x Dementia (80+)

Teremos que escolher entre morrer do coração x demenciar???

Journal of the American College of Cardiology

Subclinical Cardiovascular Disease and Death, Dementia, and Coronary Heart Disease in Patients 80+ Years

Lewis H. Kuller, MD, DRPH; Oscar L. Lopez, MD; Rachel H. Mackey, PHD, MPH; Caterina Rosano, MD, MPH; Daniel Edmundowicz, MD; James T. Becker, PHD; Anne B. Newman, MD, MPH

Disclosures

J Am Coll Cardiol. 2016;67(9):1013-1022. 

Abstract and Introduction

Abstract

Background The successful prevention and treatment of coronary heart disease (CHD) and stroke has resulted in a substantial increase in longevity, with subsequent growth in the population of older people at risk for dementia.

Objectives The authors evaluated the relationship of coronary and other peripheral atherosclerosis to risk of death, dementia, and CHD in the very elderly. Because the extent of vascular disease differs substantially between men and women, sex- and race-specific analyses were included, with a specific focus on women with low coronary artery calcium (CAC) Agatston scores.

Methods We evaluated the relationship between measures of subclinical cardiovascular disease (CAC, carotid intimal medial thickness, stenosis, and ankle brachial index) and risk of dementia, CHD, and total mortality in 532 participants of the Cardiovascular Health Study-Cognition Study from 1998/1999 (mean age, 80 years) to 2012/2013 (mean age, 93 years).

Results Thirty-six percent of participants had CAC scores >400. Women and African-Americans had lower CAC scores. Few men had low CAC scores. CAC score and number of coronary calcifications were directly related to age-adjusted total mortality and CHD. The age-specific incidence of dementia was higher than for CHD. Only about 25% of deaths were caused by CHD and 16% by dementia. Approximately 64% of those who died had a prior diagnosis of dementia. White women with low CAC scores had a significantly decreased incidence of dementia.

Conclusions In subjects 80+ years of age, there is a greater incidence of dementia than of CHD. CAC, as a marker of atherosclerosis, is a determinant of mortality, and risk of CHD and myocardial infarction. White women with low CAC scores had a significantly decreased risk of dementia. A very important unanswered question, especially in the very elderly, is whether prevention of atherosclerosis and its complications is associated with less Alzheimer disease pathology and dementia. (Cardiovascular Health Study [CHS]; NCT00005133)
************************

Conclusions

A very important unanswered question is whether 0 or very low CAC scores or other measures of lower extent of atherosclerosis or arteriosclerosis are associated with reduced risk of incident dementia. Interventions to modify known risk factors to prevent the progression of atherosclerosis and arteriosclerosis could result in a decreased older-age incidence of CHD, CVD, and dementia. The alternative could be an unfortunate outcome: that successful control of risk factors and treatment of CHD results in an increasing epidemic of dementia among older people.

DM and sub-clinical Myocardial Damage

• Original Article
  • Epidemiology and Prevention

Diabetes Mellitus, Prediabetes, and Incidence of Subclinical Myocardial Damage

1. Elizabeth Selvin, PhD, MPH; et al.

1. From the Department of Epidemiology and the Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (E.S., M.L., Y.C., L.S., J.W.M., A.R.S., J.C.); Division of General Internal Medicine, Department of Medicine, Johns Hopkins University, Baltimore, MD (E.S., M.L., J.R., J.C.); Department of Medicine, Baylor College of Medicine and Methodist DeBakey Heart and Vascular Center, Houston, TX (R.C.H., C.M.B.).

1. Correspondence to Elizabeth Selvin, PhD, MPH, Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Bloomberg School of Public Health, 2024 E Monument St, Suite 2–600, Baltimore, MD 21287. E-maileselvin@jhu.edu

 

Next Section

Abstract

Background—Persons with prediabetes and diabetes mellitus are at high risk for cardiovascular events. However, the relationships of prediabetes and diabetes mellitus to the development of subclinical myocardial damage are unclear.

Methods and Results—We measured cardiac troponin T with a highly sensitive assay (hs-cTnT) at 2 time points, 6 years apart, among 9051 participants of the community-based Atherosclerosis Risk in Communities Study with no diabetes mellitus, or prediabetes, and without cardiovascular disease including silent myocardial infarction by ECG. First, we examined the incidence of elevated hs-cTnT (≥14 ng/L) at 6 years of follow-up. Second, we examined clinical outcomes during the subsequent ≈14 years of follow-up among persons with and without incident elevations in hs-cTnT. Cumulative probabilities of elevated hs-cTnT at 6 years among persons with no diabetes mellitus, prediabetes, and diabetes mellitus were 3.7%, 6.4%, and 10.8%, respectively. Compared with normoglycemic persons, the adjusted relative risks for incident elevated hs-cTnT were 1.40 (95% CI, 1.08–1.80) for prediabetes and 2.47 (95% CI, 1.78–3.43) for diabetes mellitus. Persons with diabetes mellitus and incident elevations in hs-cTnT were at a substantially higher risk of heart failure (hazard ratio, 6.37 [95% CI, 4.27–9.51]), death (hazard ratio, 4.36 [95% CI, 3.14–6.07]), and coronary heart disease (hazard ratio, 3.84 [95% CI, 2.52–5.84]) compared with persons without diabetes mellitus and no incident elevation in hs-cTnT.

Conclusions—Prediabetes and diabetes mellitus were independently associated with the development of subclinical myocardial damage, as assessed by hs-cTnT, and those persons with evidence of subclinical damage were at highest risk for clinical events. These results support a possible deleterious effect of hyperglycemia on the myocardium, possibly reflecting a microvascular cause.

FLU and CHD

Comentário enviado pela AMICOR Maria Inês Reinert Azambuja para a Revista Science a propósito de sua contribuição original.
Ela comenta que o título remete à teoria que ela publicou em 2009 -  de que a reciclagem dos virus influenza em co-evolução com a população humana resulta em variação temporal na distribuição de fenotipos imunoinflamatórios na população, o que explica a variação temporal nos niveis e principais causas de mortalidade e a ocorrência de epidemias por diferentes doenças. Afirma que seu trabalho é consultado com bastante regularidade conforme estatísticas do ResearchGate e ela  teme que a ideia seja paulatinamente introduzida na " mainstream"  sem referência à autoria, como se simplesmente tivesse se cristalizado do nada no pensamento coletivo, ao invés de como realmente foi - fruto de quase de 20 anos de trabalho duro. 

Your comment on Flu survivors are an inflammatory club has been approved and
is now live at
http://comments.sciencemag.org/content/10.1126/science.345.6202.1307-c,

Dear Editor
The title given to this editor's choice note called my attention. Still more
after I read the note and found no relation between the note and the title.
It could well be a journalistic translation (much simplified) of an
epidemiologic theory that I advanced 5 years ago in a paper that, according
to ResearchGate stats, has been frequently accessed by colleagues around the
world.
I proposed that the recycling of influenza A viruses in co-evolution with
human populations results in an ever-changing population mixture of
individuals’ immune-inflammatory phenotypes, secularly expressed as changes
in level and distribution of causes of deaths, including epidemics/pandemics
by different diseases (1).
I am afraid that my idea might be finnaly entering the mainstram as one of
those ideas that suddenly "materializes" within the collective thought,
without reference to authorship. The theory is important, even revolutionary
in terms of our understanding of diseases causation. And it is fruit of many
years of hard work(10):
In 1992, when the diet-heart hypothesis and the degenerative paradigm were
the only possible frameworks to any explanation to the rise and fall in CHD
mortality, I finished the first draft of my hypothesis paper, showing a
birth-cohort association between the (young-adult) population with higher
mortality in the 1918 Influenza Pandemic and the (middle-age) population with
highest CHD mortality during the 1950 and 60s. In 1994, I first presented the
association publically, as a poster, in a meeting on Atherosclerosis, and
mine was the only abstract mentioning infection. In 1998 I presented it again
(as a poster), in the first world Meeting on Infection and Atherosclerosis,
and mine was the only abstract mentioning Influenza. In 2003, in the first
meeting on Influenza and Coronary Heart Disease, mine was the only study
dealing with Influenza not just as a trigger to an acute CHD event, but also
as an early-life determinant of vulnerability to triggering upon
re-infection, a much more complex idea of disease causation. In 2009, in a
multi-disciplinary conference on mortality and longevity held in Edinburgh, I
presented an updated version extended to the full theory summarized above.

(1) Azambuja MI 2009. Influenza Recycling and secular trends in mortality and
natality. British Actuarial Journal 15, Supplement, 123-150.
(2) Azambuja MI 2010 Inflammation as the cause of Coronary Heart Disease.
Lancet Inf Dis 10: 143-143.

Fat and Heart Disease

Study Questions Fat and Heart Disease Link

By ANAHAD O'CONNOR

Smokey Bones Bar & Fire Grill/PRNewsFotoA new study questions the relationship between heart disease and saturated fat.

• E-MAIL
• FACEBOOK
• TWITTER
• SAVE
• MORE

Many of us have long been told that saturated fat, the type found in meat, butter and cheese, causes heart disease. But a large and exhaustive new analysis by a team of international scientists found no evidence that eating saturated fat increased heart attacks and other cardiac events.

The new findings are part of a growing body of research that has challenged the accepted wisdom that saturated fat is inherently bad for you and will continue the debate about what foods are best to eat.

For decades, health officials have urged the public to avoid saturated fat as much as possible, saying it should be replaced with the unsaturated fats in foods like nuts, fish, seeds and vegetable oils.

But the new research, published on Monday in the journal Annals of Internal Medicine, did not find that people who ate higher levels of saturated fat had more heart disease than those who ate less. Nor did it find less disease in those eating higher amounts of unsaturated fat, including monounsaturated fat like olive oil or polyunsaturated fat like corn oil./.../

Percutaneous Coronary Interventions

JAMA Internal Medicine   Comparative Effectiveness of Percutaneous Coronary Interventions

These meta-analyses compare the efficacy of PCI to CABG for multivessel coronary artery disease, and to medical treatment for chronic stable angina. Coronary Artery Bypass Grafting vs Percutaneous Coronary Intervention and Long-term Mortality and Morbidity in Multivessel Disease: Meta-analysis of Randomized Clinical Trials of the Arterial Grafting and Stenting Era Percutaneous Coronary Intervention Outcomes in Patients With Stable Obstructive Coronary Artery Disease and Myocardial Ischemia Related editor’s note: Evolving Treatment Options in Coronary Artery Disease

PPI and ADMA

An Unexpected Effect of Proton Pump Inhibitors: Elevation of the Cardiovascular Risk Factor ADMA

1. Yohannes T. Ghebremariam1; 
2. Paea LePendu2; 
3. Jerry C. Lee2;
4. Daniel A. Erlanson2; 
5. Anna Slaviero3; 
6. Nigam H. Shah2; 
7. James Leiper3;
8. John P. Cooke1*

+Author Affiliations

1. ¹Texas Methodist Hospital Research Institute, Houston, TX
2. ²Stanford University, Stanford, CA
3. ³MRC Clinical Sciences Center, Imperial College London, London, UK

1. ↵* Department of Cardiovascular Sciences, Texas Methodist Research Institute, Houston TX, 77030 john.cooke@stanford.edu

Abstract

Background—Proton pump inhibitors (PPIs) are gastric acid suppressing agents widely prescribed for the treatment of gastro-esophageal reflux disease (GERD). Recently, several studies in patients with acute coronary syndrome (ACS) have raised the concern that use of PPIs in these patients may increase their risk of major adverse cardiovascular events (MACE). The mechanism of this possible adverse effect is not known. Whether the general population might also be at risk has not been addressed.

Methods and Results—Plasma ADMA is an endogenous inhibitor of nitric oxide synthase (NOS). Elevated plasma ADMA is associated with increased risk for cardiovascular disease, likely due to its attenuation of the vasoprotective effects of endothelial NOS. We find that PPIs elevate plasma asymmetric dimethylarginine (ADMA) level and reduce nitric oxide (NO) levels and endothelium-dependent vasodilation in a murine model and ex vivo human tissues. PPIs increase ADMA because they bind to, and inhibit dimethylarginine dimethylaminohydrolase (DDAH), the enzyme that degrades ADMA.

Conclusions—We present a plausible biological mechanism to explain the association of PPIs with increased MACE in patients with unstable coronary syndromes. Of concern, this adverse mechanism is also likely to extend to the general population using PPIs. This finding compels additional clinical investigations and pharmacovigilance directed toward understanding the cardiovascular risk associated with use of the PPIs in the general population.

AHA Guidelines IHD

  2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and  Management of Patients With Stable Ischemic Heart Disease: A Report of
  the American College of Cardiology Foundation/American Heart Association
  Task Force on Practice Guidelines, and the American College of
  Physicians, American Association for Thoracic Surgery, Preventive
  Cardiovascular Nurses Association, Society for Cardiovascular Angiography
  and Interventions, and Society of Thoracic Surgeons
  Stephan D. Fihn, Julius M. Gardin, Jonathan Abrams, Kathleen Berra, James
  C. Blankenship, Apostolos P. Dallas, Pamela S. Douglas, JoAnne M. Foody,
  Thomas C. Gerber, Alan L. Hinderliter, Spencer B. King III, Paul D.
  Kligfield, Harlan M. Krumholz, Raymond Y.K. Kwong, Michael J. Lim, Jane
  A. Linderbaum, Michael J. Mack, Mark A. Munger, Richard L. Prager, Joseph
  F. Sabik, Leslee J. Shaw, Joanna D. Sikkema, Craig R. Smith, Jr, Sidney
  C. Smith, Jr, John A. Spertus, and Sankey V. Williams
  Circulation. Originally published November 19, 2012. doi:
  10.1161/CIR.0b013e318277d6a0
  http://circ.ahajournals.org/content/early/2012/11/19/CIR.0b013e318277d6a0.full.pdf?papetoc


  2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and
  Management of Patients With Stable Ischemic Heart Disease: Executive  Summary: A Report of the American College of Cardiology
  Foundation/American Heart Association Task Force on Practice Guidelines,
  and the American College of Physicians, American Association for Thoracic
  Surgery, Preventive Cardiovascular Nurses Association, Society for
  Cardiovascular Angiography and Interventions, and Society of Thoracic
  Surgeons
  Stephan D. Fihn, Julius M. Gardin, Jonathan Abrams, Kathleen Berra, James
  C. Blankenship, Apostolos P. Dallas, Pamela S. Douglas, JoAnne M. Foody,
  Thomas C. Gerber, Alan L. Hinderliter, Spencer B. King III, Paul D.
  Kligfield, Harlan M. Krumholz, Raymond Y.K. Kwong, Michael J. Lim, Jane
  A. Linderbaum, Michael J. Mack, Mark A. Munger, Richard L. Prager, Joseph
  F. Sabik, Leslee J. Shaw, Joanna D. Sikkema, Craig R. Smith, Jr, Sidney
  C. Smith, Jr, John A. Spertus, and Sankey V. Williams
  Circulation. Originally published November 19, 2012. doi:
  10.1161/CIR.0b013e3182776f83
  http://circ.ahajournals.org/content/early/2012/11/19/CIR.0b013e3182776f83.full.pdf?papetoc

Type O Blood x CHD

Type O Blood Carries Lower CHD Risk

By Cole Petrochko, Associate Staff Writer, MedPage Today

Published: August 14, 2012

Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco

Action Points

• Patients with type A, B, or AB blood are at significantly greater risk for coronary heart disease (CHD) than those with type O blood, a study has found.
• Note that the associations between blood type and CHD risk were not modified by age, physical activity, alcohol consumption, smoking status, or diabetes history in men or women.

Patients with type A, B, or AB blood are at significantly greater risk for coronary heart disease (CHD) than those with type O blood, researchers found.

Two large, prospective cohort studies showed those with a non-O blood type had an age-adjusted hazard ratio of 1.09 (95% CI 1.03 to 1.17, P=0.005) for risk of developing CHD, according to Lu Qi, PhD, of the Harvard School of Public Health, and colleagues.

A meta analysis of an additional six past cohorts also showed a significant pooled relative risk for CHD in patients with non-O blood type of 1.11 (95% CI 1.05 to 1.18, P=0.001), Qi and co-authors wrote in the August 14 issue ofArteriosclerosis, Thrombosis, and Vascular Biology./.../