‘Tis The Coronary Season

 

# 9471

 

If history is any gauge the three deadliest coronary days of the year will occur over the next two weeks; Christmas day, the day after Christmas, and New Year’s Day.   Events that are commonly called `Christmas Coronaries’ or `Hanukkah Heart Attacks’.

 

Fifteen years ago, a study looked at the rate of heart attacks in the United States, and found that Acute Myocardial Infarctions (AMIs) run as much 53% higher during the winter months than than during the summer.

 

Seasonal distribution of acute myocardial infarction in the second National Registry of Myocardial Infarction.

Spencer FA, Goldberg RJ, Becker RC, Gore JM.

 

While cold weather combined with strenuous physical activity (like clearing snow from sidewalks) has often been blamed for this spike, even in balmy Southern California, studies have shown a 33% increase in heart attacks over the holidays (see below).

When Throughout the Year Is Coronary Death Most Likely to Occur?

A 12-Year Population-Based Analysis of More Than 220 000 Cases

Robert A. Kloner, MD, PhD; W. Kenneth Poole, PhD; Rebecca L. Perritt, MS

Non-climate related factors – like over indulgence in food and alcohol, diminished activity levels, forgetting to take prescription medicines, and combined holiday stressors like shopping, running up debt, traveling, meal preparation, and the angst that comes from dysfunctional family gatherings are likely contributors to this yearly spike. 

 

But increasingly influenza and other respiratory infections have been linked to this seasonal increase in heart attacks.

 

In 2012, in Study: Influenza And Heart Attacks, we looked at research that appeared in the Journal of Infectious Diseases that suggested Influenza - and other acute respiratory infections - can act as a trigger for heart attacks. The same issue carried an editorial called Increasing Evidence That Influenza Is a Trigger for Cardiovascular Disease.

 

Influenza Infection and Risk of Acute Myocardial Infarction in England and Wales: A CALIBER Self-Controlled Case Series Study

Charlotte Warren-Gash, Andrew C. Hayward1, Harry Hemingway2, Spiros Denaxas2, Sara L. Thomas3, Adam D. Timmis5, Heather Whitaker6 and Liam Smeeth4

In 2010, in CMAJ: Flu Vaccinations Reduce Heart Attack Risk we saw what would turn out to be a controversial study (see Vaccine/Heart Attack Study Questioned) that strongly suggested that those over the age of 40 who get a seasonal flu vaccine each year may reduce their risk of a heart attack by as much as 19%.

 

Last year (October 2013), in JAMA: Flu Vaccine and Cardiovascular Outcomes, we looked at a meta-analysis of  5 published and 1 unpublished randomized clinical trials involving  6735 patients – that found among those who had previously had a heart attack, the receipt of a flu vaccine was linked to a 55% reduction in having another major cardiac event in the next few months.

 

So the idea that heart attacks may be linked to influenza infection is hardly new.

 

In late October of this year, the Texas Heart Institute published this article, suggesting that tens of thousands of cardiac deaths could be prevented if every high-risk cardiac patient got the flu shot each year.

 

Research Shows Flu Can Trigger Heart Attacks

Influenza vaccinations could prevent thousands of deaths from heart disease

People who are at risk of heart disease should receive the influenza vaccine every autumn. Research shows that influenza epidemics are associated with a rise in deaths from heart disease and that flu can actually trigger the heart attacks that result in death.

However, only about 60 percent of people in the U.S. who ought to have a flu vaccination actually have one, said Mohammad Madjid, MD, MSc, a senior research scientist at the Atherosclerosis Research Lab of the Texas Heart Institute.

(Continue . . . )

 

If their hypothesis is correct – given the expected reduced effectiveness of this year’s flu vaccine (see CDC HAN Advisory On `Drifted’ H3N2 Seasonal Flu Virus) and the rising tide of H3N2 influenza across the country – the next couple of weeks could prove very busy for the nation’s EMS crews and Coronary care units.

But regardless of the effectiveness of this year’s flu shot, and influenza’s effects on cardiovascular events, even on an `average day’ roughly 1,000 people suffer a Sudden Cardiac Arrest (SCA) in the United States.

 

This from the Heart Rhythm Association:

• Sudden Cardiac Arrest (SCA) is a leading cause of death in the United States, claiming more than 350,000 lives each year.
• Approximately 92% of those who experience sudden cardiac arrest do not survive.
• SCA kills more than 1,000 people a day, or one person every 90 seconds

 

What the people who witness these events do in the first few minutes can mean the difference between life and death for the stricken individual. Luckily, hands-only CPR (cardio-pulmonary resuscitation) is easier to do than ever before, and there are thousands of AEDs (automated external defibrillators) stationed in public venues across the nation.

 

With a little bit of training, you have the potential to save someone’s life.

 

While it won’t take the place of an actual class, you can watch how it is done on in this brief instructional video from the American Heart Association.  To learn how to use an AED, you can use this online training module  I wrote about in CPR Skills & AED Simulator.  A  CPR class only takes a few hours, can be fun, and is well worth the effort.  

 

To find a local CPR course contact your local chapter of the American Red Cross, the American Heart Association, or (usually) your local fire department or EMS can steer you to a class.

 

Of course, despite your best efforts, many SCA victims will not survive. It isn’t at all like on TV, where 75% of  recipients of CPR survive.  Even when cardiac arrests occur inside a hospital, the survival to discharge rate is less than 40%. Outside the hospital, the odds of seeing a good outcome are lower.

 

While there are no guarantee of success, early and coordinated action taken by bystanders (calling 911, starting CPR, using AED if available) can substantially improve the SCA’s chances of survival. 

 

For more on heart attacks, and CPR, you may wish to visit some of these earlier blogs.

 

Deadlier Than For The Male

Survivability Of Non-Shockable Rhythms With New CPR Guidelines

Fear Of Trying

NPM11: Early CPR Saves Lives

mBio: Biofilms, Stress Hormones & Heart Attacks

Diseased Carotid Arteries - Credit: David Davies, University of Binghamton

 

 

# 8729

 

A couple of months ago, in Post-Disaster Stress Cardiomyopathy: A Broken-Hearted Malady, we looked at a study that found a significant increase in a very rare type of heart problem called Takotsubo cardiomyopathy – also known as broken heart syndrome – following high impact natural disasters.

 

This stress related syndrome causes acute ballooning of the heart ventricles, and is a well-recognized cause of acute heart failure and dangerous cardiac arrhythmias.  

 

Johns Hopkins Medicine has a Frequently Asked Questions about Broken Heart Syndrome, that describes the condition:

1. What is “stress cardiomyopathy?”

Stress cardiomyopathy, also referred to as the “broken heart syndrome,” is a condition in which intense emotional or physical stress can cause rapid and severe heart muscle weakness (cardiomyopathy). This condition can occur following a variety of emotional stressors such as grief (e.g. death of a loved one), fear, extreme anger, and surprise. It can also occur following numerous physical stressors to the body such as stroke, seizure, difficulty breathing (such as a flare of asthma or emphysema), or significant bleeding.

 

We’ve looked at other post-disaster (likely stress related) cardiac problems, including earlier last March in Tulane University: Post-Katrina Heart Attack Rates – Revisited, where an ongoing study finds that heart attack rates remain elevated by 300% in New Orleans six years after that hurricane struck.

 

While there is plenty of anecdotal evidence showing that stress, fear, grief, or other emotional stressors can cause sudden heart attacks thus far we haven’t had a good model as to how that might happen.

 

Yesterday the open access journal mBio published a fascinating bit of work that attempts to show how a sudden release of the right stress hormone (norepinephrine) can dissolve bacteria laden biofilm deposits in the carotid artery, potentially initiating a heart attack or stroke.

 

Bacteria Present in Carotid Arterial Plaques Are Found as Biofilm Deposits Which May Contribute to Enhanced Risk of Plaque Rupture

Bernard B. Lanter, Karin Sauer, David G. Davies

IMPORTANCE The association of bacteria with atherosclerosis has been only superficially studied, with little attention focused on the potential of bacteria to form biofilms within arterial plaques.

In the current work, we show that bacteria form biofilm deposits within carotid arterial plaques, and we demonstrate that one species we have identified in plaques can be stimulated in vitro to undergo a biofilm dispersion response when challenged with physiologically relevant levels of norepinephrine in the presence of transferrin. Biofilm dispersion is characterized by the release of bacterial enzymes into the surroundings of biofilm microcolonies, allowing bacteria to escape the biofilm matrix.

We believe these enzymes may have the potential to damage surrounding tissues and facilitate plaque rupture if norepinephrine is able to stimulate biofilm dispersion in vivo. This research, therefore, suggests a potential mechanistic link between hormonal state and the potential for heart attack and stroke.

(Continue . . . )

 

The American Society for Microbiology has a press release that explains in layman’s terms the mechanism this study believes it has discovered.

 

Bacteria help explain why stress, fear trigger heart attacks

WASHINGTON, DC – June 10, 2014 - Scientists believe they have an explanation for the axiom that stress, emotional shock, or overexertion may trigger heart attacks in vulnerable people. Hormones released during these events appear to cause bacterial biofilms on arterial walls to disperse, allowing plaque deposits to rupture into the bloodstream, according to research published in published today in mBio®, the online open-access journal of the American Society for Microbiology.

"Our hypothesis fitted with the observation that heart attack and stroke often occur following an event where elevated levels of catecholamine hormones are released into the blood and tissues, such as occurs during sudden emotional shock or stress, sudden exertion or over-exertion" said David Davies of Binghamton University, Binghamton, New York, an author on the study.

Davies and his colleagues isolated and cultured different species of bacteria from diseased carotid arteries that had been removed from patients with atherosclerosis. Their results showed multiple bacterial species living as biofilms in the walls of every atherosclerotic (plaque-covered) carotid artery tested.

In normal conditions, biofilms are adherent microbial communities that are resistant to antibiotic treatment and clearance by the immune system. However, upon receiving a molecular signal, biofilms undergo dispersion, releasing enzymes to digest the scaffolding that maintains the bacteria within the biofilm. These enzymes have the potential to digest the nearby tissues that prevent the arterial plaque deposit from rupturing into the bloodstream.

According to Davies, this could provide a scientific explanation for the long-held belief that heart attacks can be triggered by a stress, a sudden shock, or overexertion

(Continue . . .)

 

All of this is a very simplistic summation of a complex, and fascinating paper, one that many will want to read in its entirety. While far from settled science, it proffers a very interesting avenue for further investigation. 

Of note, while some heart attacks and Takotsubo cardiomyopathy are thought to be induced by similar cascades of stress-related hormones, their actual physical effects appears to be quite different.  Johns Hopkins describes the theories behind the cause of stress-cardiomyopathy below:

 

The precise way in which adrenaline affects the heart is unknown. It may cause narrowing of the arteries that supply the heart with blood, causing a temporary decrease in blood flow to the heart. Alternatively, the adrenaline may bind to the heart cells directly causing large amounts of calcium to enter the cells which renders them temporarily dysfunctional.

 

The bottom line, I suppose, is that by whatever mechanism, overwhelming stress can take a heavy toll on our physical and mental health.

And in ways that we are only just now beginning to unravel.

Tulane University: Post-Katrina Heart Attack Rates - Revisited

Hurricane Katrina Approaching New Orleans August 2005

 

# 8388

 

In March of 2009, in a study led by Dr. Anand Irimpen (Associate Professor of clinical medicine at Tulane), it was disclosed that residents of New Orleans saw a 300% increase in heart attacks in the first 2 years after hurricane Katrina.

 

The Tulane University news NEW WAVE carried this report in 2009.

Post-Katrina Stress, Heart Problems Linked

March 30, 2009

(Excerpt)

There were 246 admissions for heart attacks, out of a total census of 11,282 patients, post-Katrina compared with 150 admissions out of a total 21,229 patients in the two years before the storm. In addition to a three-fold increase in heart attacks and a 120 percent increase in coronary interventions, the post-Katrina group had significantly higher prevalence of unemployment, lack of medical insurance, medication noncompliance, smoking, substance abuse, first-time hospitalization and people living in temporary housing. There were no significant differences in the racial, gender or age distribution of the two groups.

 

In 2011, we looked at an update to this Tulane study (see Post-Katrina Heart Attack Rates) that found – four years after the disaster – that heart attack rates remained 300% higher than pre-Katrina levels in the City, and that:

 

While psychiatric conditions such as clinical depression, a history of coronary artery disease and marital status did not appear to contribute to heart attacks in the two-year analysis, these factors seem to play a significant role as time has progressed.

Irimpen suggests there is a lag phase between the onset of psychiatric illness and its manifestation in the form of a heart attack. 

Today, Tulane University has announced a 6-year follow up to this study, and once again the impact of Katrina on cardiac health remains pronounced.  First some details on the study, after which I’ll return with more:

 

Rise in Heart Attacks After Hurricane Katrina Persisted Six Years Later

Researchers also find a lasting disruption in the timing of heart attacks after the disaster.

Released: 3/18/2014 10:00 AM EDT
Source Newsroom: Tulane University

Mayo Clinic Proceedings

Newswise — Lingering stress from major disasters can damage health years later, according to a new Tulane University study that found a three-fold spike in heart attacks continued in New Orleans six years after Hurricane Katrina.

Researchers also found a lasting disruption in the timing of heart attacks in the six years after the storm with significantly more incidents occurring on nights and weekends, which are typically times hospitals see fewer admissions for heart attacks.

The research, which will be published in the journal Mayo Clinic Proceedings, is an update of an ongoing study tracking the increases in admissions for heart attacks at Tulane Medical Center in downtown New Orleans after Hurricane Katrina. The new study confirmed the increase persisted even six years later.

“Prior to Hurricane Katrina, about 0.7 percent of the patients we were treating in our medical center were suffering from myocardial infarctions (heart attacks),” said lead author Dr. Matthew Peters, internal medicine resident at Tulane University School of Medicine. “This increased to about 2 percent in first three years after Katrina and continued to increase to almost 3 percent in years four through six after the storm.”

The hospital had 1,177 heart attack cases during the six years after the storm, representing 2.4 percent of patient admissions; only 0.7 percent of its patients were admitted for heart attacks two years before Katrina.

Researchers attribute the increase to several factors, most notably chronic stress, higher unemployment and greater risk factors for heart disease, such as increased rates of smoking, substance abuse, psychiatric disorders and noncompliance in taking prescribed medications.

“We found more patients without insurance, who were unemployed and more who had a previous history of coronary artery disease, showing us that the milieu of patients was a sicker population,” said senior author Dr. Anand Irimpen, an associate professor of medicine for the Tulane Heart and Vascular Institute and chief, cardiology section, Southeast Louisiana Veterans Health Care System.

Video interviews with both researchers are available online:

Dr. Matthew Peters – http://youtu.be/2oPOUZZLOmE

Dr. Anand Irimpen - http://youtu.be/nWANLTsSnzY

 

We’ve looked at other post-disaster health impacts in the past, such as in Post Disaster Stress & Suicide Rates. One disaster discussed was a 1999 7.3 earthquake that struck in Chi-Chi, Nantou county in central Taiwan killing more than 2,300 people.

 

A study that subsequently appeared in the Taiwan Journal of Medicine (Disease-specific Mortality Associated with Earthquake in Taiwan Hsien-Wen Kuo, Shu-Jen Wu, Ming-Chu Chiu) found `a considerable increase in the number of suicides after the earthquake’.

 

A little over a year ago, in Disaster’s Hidden Toll, we looked at the long-term, largely unseen, effect on nursing home patients who were forced to evacuate to temporary facilities after Japan’s Great Earthquake & Tsunami of 2011.

 

A study showed a 2.4 fold increase in deaths during the 8 months following the earthquake.  Deaths not caused by the quake, tsunami, or radiation release itself – but likely brought on by the stress of having to live in make-shift emergency shelters.

 

And just last month, in The Long Term Effects Of A Major Disaster, we looked at the post-tsunami deaths due to stress and displacement that exceeded – at least in one prefecture – those experienced during the initial earthquake and tsunami.

 

Closer to home, last fall in Sandy 1 Year Later: Coping With The Aftermath, we looked at the lingering psychological effects of New England’s brush with that late season super storm of 2012.

 

While the psychological impact of a major disaster cannot be fully prevented, individual, family, and business preparedness can go a long ways towards reducing the impact of any disaster.

 

FEMA, Ready.gov, along with organizations like the American Red Cross (and indeed, this blog), spend a great deal of time trying to convince individuals, families, businesses and communities of the value of preparing for a wide variety of emergencies and disasters.

 

Having a modest supply of food, water, and medicine – and a workable family or business disaster plan – can go a long ways toward reducing both stress and hardship during and after a disaster. The standard advice is that everyone needs to be prepared to deal with a disaster for at least 3 days (meaning having a first aid kit, emergency supplies, and a plan) before help arrives.

 

Sure . . .  they’d like you to be prepared for longer . . .  but 72 hours is a reasonable start. I personally advocate having 2 week’s worth of supplies, but then I live in the heart of hurricane country, and have a fondness for eating regularly (see NPM11: Living The Prepared Life). 

 

Although a good disaster plan and emergency kit are imperative to get you through the opening hours, days, or even weeks of a disaster, knowing how to help friends, family, and neighbors deal with the psychological effects of a disaster can be equally important.

 

While often hidden from view, the psychological impact of a disaster can be enormous and ongoing. Last year in Post Disaster Stress & Suicide Rates we looked at the impact of disaster-related PTSD (Post Traumatic Stress Disorder). Luckily, there are things that can be done - even by the layperson - to help reduce the psychological impact of a disaster. 

 

A few resources you may wish to revisit:

 

In Psychological First Aid: The WHO Guide For Field Workers we looked a simple guidebook anyone can use to help others in emotional distress.

 

The CDC also provides a website which contains a number of resources devoted to coping with disasters.

 

Coping With a Disaster or Traumatic Event

Trauma and Disaster Mental Health Resources

The effects of a disaster, terrorist attack, or other public health emergency can be long-lasting, and the resulting trauma can reverberate even with those not directly affected by the disaster. This page provides general strategies for promoting mental health and resilience. These strategies were developed by various organizations based on experiences in prior disasters.

 

Last August the World Health Organization released a comprehensive Guidelines For Post-Trauma Mental Health Care book on the treatment of PTSD, acute stress, and bereavement:

The bottom line is that those who follow FEMA’s, and Ready.gov’s advice to Have A Plan, Make A Kit, and Be informed  will be not only be better able to deal with a disaster, they will be better prepared to weather the rigors of a long recovery as well.

 

And that, in turn, could help reduce the risks of post-disaster health issues, such as has plagued New Orleans since Katrina.

 

A few of my (many) blogs on disaster preparedness include:

In An Emergency, Who Has Your Back?

When 72 Hours Isn’t Enough

When Evacuation Is The Better Part Of Valor

Marital Status & Cardiac Mortality: A Matter Of Wife Or Death?

 

# 8369

 

As a retired paramedic who plied his modest skills throughout the 1970s across three notorious `cardiac cities’ (Phoenix, AZ, St. Petersburg & Bradenton, FL) – and now reaching `that age’ where I have to think about such things on a more personal level -  I have more than a passing interest in heart disease and heart attacks.

 

There’s been a good deal of research to show that married men live longer than their divorced or unmarried counterparts (see Harvard Health Watch Marriage and men's health), but far less is known about the health effects of marriage for women.

 

We’ve an open access study today, published in the journal BMC Medicine, that attempts to answer this question – at least in regards to Ischemic Heart Disease (IHD).  Utilizing the vast stores of data accumulated from the UK's Million Women Study - a comprehensive survey of more than 1.3 million women aged 50 or older recruited between 1996 and 2001- researchers were able to include data from more than 700,000 women in their study.

 

While they found that women who were married (or living with a partner) had the same risk of developing heart disease as single women, they found that women with partners were 28% less likely to die from heart disease.

 

First, a look at the abstract (the entire study is available at the link below), then I’ll be back with a bit more.

 

Marital status and ischemic heart disease incidence and mortality in women: a large prospective study

Sarah Floud^*, Angela Balkwill, Dexter Canoy, F Lucy Wright, Gillian K Reeves, Jane Green, Valerie Beral, Benjamin J Cairns and the Million Women Study Collaborators

Abstract

Background

Being married has been associated with a lower mortality from ischemic heart disease (IHD) in men, but there is less evidence of an association for women, and it is unclear whether the associations with being married are similar for incident and for fatal IHD. We examined the relation between marital status and IHD incidence and mortality in the Million Women Study.

Methods

A total of 734,626 women (mean age 60 years) without previous heart disease, stroke or cancer, were followed prospectively for hospital admissions and deaths. Adjusted relative risks (RRs) for IHD were calculated using Cox regression in women who were married or living with a partner versus women who were not. The role of 14 socio-economic, lifestyle and other potential confounding factors was investigated.

Results

81% of women reported being married or living with a partner and they were less likely to live in deprived areas, to smoke or be physically inactive, but had a higher alcohol intake than women who were not married or living with a partner. During 8.8 years of follow-up, 30,747 women had a first IHD event (hospital admission or death) and 2,148 died from IHD. Women who were married or living with a partner had a similar risk of a first IHD event as women who were not (RR = 0.99, 95% confidence interval (CI) 0.96 to 1.02), but a significantly lower risk of IHD mortality (RR = 0.72, 95% CI 0.66 to 0.80, P <0.0001). This lower risk of IHD death was evident both in women with and without a prior IHD hospital admission (respectively: RR = 0.72, 95% CI 0.60 to 0.85, P <0.0001, n = 683; and 0.70, 95% CI 0.62 to 0.78, P <0.0001, n = 1,465). These findings did not vary appreciably between women of different socio-economic groups or by lifestyle and other factors.

Conclusions

After adjustment for socioeconomic, lifestyle and other factors, women who were married or living with a partner had a similar risk of developing IHD but a substantially lower IHD mortality compared to women who were not married or living with a partner.

 

While this is likely the largest study of this kind, it is not the first to show that married men and women tend to outlive those who live alone.

 

Roughly a year ago, a Finnish study, published in the European Journal of Preventive Cardiology found that both men and women who lived alone are at a higher risk of having a heart attack, and had a worse prognosis when they did. Being married (or partnered) was linked to a "considerably better prognosis of acute cardiac events both before hospitalization and after reaching the hospital alive".

 

Prognosis of acute coronary events is worse in patients living alone: the FINAMI myocardial infarction register

Aino Lammintausta1, Juhani KE Airaksinen1, Pirjo Immonen-Räihä1, Jorma Torppa2, Antero Y Kesäniemi3, Matti Ketonen4, Heli Koukkunen5,6, Päivi Kärjä-Koskenkari3, Seppo Lehto6, Veikko Salomaa2

Abstract

Background Single living has been associated with a worse prognosis of acute coronary syndrome (ACS). We aimed to study the relation of sociodemographic characteristics to the morbidity, mortality, and case fatality (CF) of ACS in a large population-based ACS register.

Methods The population-based FINAMI myocardial infarction register recorded 15,330 cases of ACS among persons aged 35–99 years in Finland in 1993–2002. Record linkage with the files of Statistics Finland provided information on sociodemographic characteristics (marital status, household size).

Results ACS incidence and 28-day mortality rate were higher in unmarried men and women in all age groups. The prehospital CF of incident ACS was higher in single living and/or unmarried 35–64-year-old people. The 28-day CF was 26% (95% confidence interval, CI, 24–29%) in married men, 42% (95% CI 37–47%) in men who had previously been married, and 51% (95% CI 46–57%) in never-married men. Among women, the corresponding figures were 20% (95% CI 15–24%), 32% (95% CI 25–39%), and 43% (95% CI 31–56%). Most of these CF differences were apparent already at the prehospital phase. The only difference in treatment was that middle-aged men living alone or unmarried received thrombolysis less often. The disparities in ACS morbidity and mortality by marital status tended to widen during the study period.

Conclusions Single living and/or being unmarried increases the risk of having a heart attack and worsens its prognosis both in men and women regardless of age. Most of the excess mortality appears already before the hospital admission and seems not to be related to differences in treatment of ACS.

 

Higher pre-hospital mortality from cardiac events among single people is likely explained – at least in part – to not having someone to call for help, or initiate CPR, in a timely fashion. But this study also found that 28-day mortality rates were significantly higher in both unmarried men (60%-168%) and  unmarried women (71%-175%) than their married counterparts.

 

Heart attacks are not – as once believed – predominantly a `male problem’.  Thirty years ago, if a man  experienced `chest pain’, doctors would immediately suspect a heart attack, but if a similarly aged woman presented with the same symptoms, they’d think first `gall bladder’. 

 

Complicating matters, women don’t always show the same classic symptoms (e.g. crushing chest pain radiating down the left arm, dyspnea, diaphoresis) that men usually do when having a heart attack. The American Heart Association’s article Heart Attack Symptoms in Women explains some of the differences.

 

In Deadlier Than For The Male, we looked at research that examined the impact of coronary heart disease on women, and differences in their symptoms and the treatment they receive.  Their conclusion: Contrary to long held beliefs, heart attacks for women can actually be deadlier than for the male.

 

Exactly why partnered people fare better when it comes to cardiac events isn’t really understood, although a number of theories (more emotional & physical support, better diet, better adherence to meds, etc.) have been proposed.  And it should also be noted that these studies focused on cardiac events and mortality.

 

Future studies are needed to look at marriage’s effects on other factors and events, such as strokes and cancer.

 

According to The American Heart Association (data for 2009) every year an estimated 785,000 Americans experience their first heart attack, and another 470,000 suffer a recurrent heart attack. They also estimate another 195,000 `silent’ myocardial infarctions occur each year.

So now would be a good time to remind my readers (partnered, or otherwise) to of the importance of learning CPR. 

Compression-only CPR is now the standard for laypeople, and so you don’t have to worry about doing mouth-to-mouth. While it won’t take the place of an actual class, you can watch how it is done on in this brief instructional video from the American Heart Association.

 

A class only takes a few hours, and it could end up helping you save the life of someone you love.

 

To find a local CPR course contact your local chapter of the American Red Cross, the American Heart Association, or (usually) your local fire department or EMS can steer you to a class.

JAMA: Flu Vaccine and Cardiovascular Outcomes

 

# 7890

 

One of the problems with determining the true burden of influenza on the public’s health is that influenza is rarely listed as the primary cause of death when a patient dies with a history of other co-morbidities like coronary artery disease, Asthma, Diabetes, or COPD.   Yet we know that during the winter months, when influenza and other respiratory viruses are at their height – overall mortality goes up. 

 

Roughly 15 years ago, a study looked at the rate of heart attacks in the United States, and found that Acute Myocardial Infarctions (AMIs) run as much 53% higher during the winter months than than during the summer. While cold weather combined with strenuous physical activity (like clearing snow from sidewalks) have often been blamed for this spike, even in balmy Southern California, studies have shown a 33% increase in heart attacks over the holidays (cite).

 

Although not the first to do so, a year ago  in Study: Influenza And Heart Attacks, we looked at research that appeared in the Journal of Infectious Diseases that suggested Influenza - and other acute respiratory infections - can act as a trigger for heart attacks.  

Despite often disappointing vaccine effectiveness (VE) numbers for those over the age of 65 (see NFID: The Challenges Of Influenza In Older Adults), in recent years we’ve seen a series of studies that have suggested that the flu vaccine may be partially protective against heart attacks. 

 

In 2010 we saw a study in the CMAJ: Flu Vaccinations Reduce Heart Attack Risk that found that those over the age of 40 who get a seasonal flu vaccine each year may reduce their risk of a heart attack by as much as 19%. Almost immediately questions were raised over the way this study was conducted (see Vaccine/Heart Attack Study Questioned). The primary concern was these researchers only looked at heart attacks during `flu season’, without the control of looking at AMI risks year-round.

 

Just last August (see Study: Flu Vaccine May Reduce Heart Attack Risk), we looked at a new study out of Australia – published in the BMJ Journal Heart, that found compelling – but not exactly conclusive – evidence that flu shots may reduce the risk of heart attacks.

 

Today, another study, which appears in JAMA, that performed a meta-analysis of  5 published and 1 unpublished randomized clinical trials involving  6735 patients - some of whom received a flu shot while others received a placebo - and calculated the number of cardiac events each group suffered in the months that followed. 

 

Among those who had previously had a heart attack, the receipt of a flu vaccine was linked to a 55% reduction in having another major cardiac event in the next few months.

 

First a link to the JAMA study, and then some excerpts from the press release from  Women's College Hospital at the University of Toronto:

 

Association Between Influenza Vaccination and Cardiovascular Outcomes in High-Risk Patients

A Meta-analysis

FREE

Jacob A. Udell, MD, MPH, FRCPC¹; Rami Zawi, MD²; Deepak L. Bhatt, MD, MPH^3,4; Maryam Keshtkar-Jahromi, MD, MPH^5,6; Fiona Gaughran, MD^7,8; Arintaya Phrommintikul, MD⁹; Andrzej Ciszewski, MD¹⁰; Hossein Vakili, MD¹¹; Elaine B. Hoffman, PhD⁴; Michael E. Farkouh, MD, MSc, FRCPC¹²; Christopher P. Cannon, MD⁴

Results Five published and 1 unpublished randomized clinical trials of 6735 patients (mean age, 67 years; 51.3% women; 36.2% with a cardiac history; mean follow-up time, 7.9 months) were included. Influenza vaccine was associated with a lower risk of composite cardiovascular events (2.9% vs 4.7%; RR, 0.64 [95% CI, 0.48-0.86], P = .003) in published trials. A treatment interaction was detected between patients with (RR, 0.45 [95% CI, 0.32-0.63]) and without (RR, 0.94 [95% CI, 0.55-1.61]) recent ACS (P for interaction = .02). Results were similar with the addition of unpublished data.

Conclusions and Relevance In a meta-analysis of RCTs, the use of influenza vaccine was associated with a lower risk of major adverse cardiovascular events. The greatest treatment effect was seen among the highest-risk patients with more active coronary disease. A large, adequately powered, multicenter trial is warranted to address these findings and assess individual cardiovascular end points.

 

 

From the press release:

Flu shot halves risk of heart attack or stroke in people with history of heart attack, study finds

TORONTO, ON, October 22, 2013 — The flu vaccine may not only ward off serious complications from influenza, it may also reduce the risk of heart attack or stroke by more than 50 per cent among those who have had a heart attack, according to new research led by Dr. Jacob Udell, a cardiologist at Women's College Hospital and clinician-scientist at the University of Toronto. What's more, the vaccine's heart protective effects may be even greater among those who receive a more potent vaccine.

"Our study provides solid evidence that the flu shot helps prevent heart disease in vulnerable patients —with the best protection in the highest risk patients," Dr. Udell said. "These findings are extraordinary given the potential for this vaccine to serve as yearly preventative therapy for patients with heart disease, the leading cause of death among men and women in North America."

Published today in the Journal of the American Medical Association, the study reviewed six clinical trials on heart health in people who received the flu vaccine. The studies included more than 6,700 patients with a history of heart disease. The researchers found people who received the flu shot:

• Had a 36 percent lower risk of a major cardiac event (heart attack, stroke, heart failure, or death from cardiac–related causes) one year later
• Had a 55 percent lower risk of a major cardiac event if they had a recent heart attack
• Were less likely to die from cardiac-related and other causes, and
• Were less likely to have a major cardiac event with a more potent vaccine compared with the standard seasonal vaccine

(Continue . . .)

 

While not a slam dunk (larger, more robust more studies are needed), this latest report adds to the body of evidence suggesting that influenza contributes significantly to cardiovascular events, and that flu vaccines may be useful in reducing cardiac mortality rates. 

I’m fully cognizant of the limitations of today’s flu vaccines, and try not to `oversell’  them in this blog. Nevertheless, I get one every year and urge that others do the same.

 

Not because they are 100% protective.  They aren’t. But they do offer moderate levels of protection (see CIDRAP: A Comprehensive Flu Vaccine Effectiveness Meta-Analysis), and have an excellent safety profile. 

 

We take sensible precautions every day – like buckling up when we drive, or wearing a helmet when we bike. None of these provide a 100% guarantee of avoiding injury, but they make sense because they increase our odds of walking away from an accident.   

 

I view getting a yearly flu shot in much the same way. 

The Emergency Oxygen Debate: Revisited

Photo Credit – Wikipedia Commons

 

# 7825

 

Supplemental oxygen has been a mainstay treatment by emergency rooms, ICUs, paramedics, and EMTs for decades, and is most often employed for shortness of breath and/or chest pain.  But, as my old paramedic instructor warned more than 40 years ago, `Oxygen is a drug.  And if administered improperly, can do more harm than good.”

 

The primary concern (four decades ago) was that patients with COPD receiving too much oxygen would suffer respiratory failure.   The rule of thumb was no more than 2 to 3 liters of O2 for an emphysema (COPD) patient.

 

Sometime in the mid-1980s, the thinking changed, and it became standard  protocol for a lot of EMS services not to deprive COPD patients in serious respiratory distress of high flow rates of oxygen. Running contrary to that opinion, in 2008 the British Thoracic Society came up with guidelines that restricted in-the-field oxygen delivery for COPD patients – and those were adopted by British Ambulance services in 2009.

 

That guideline recommended that oxygen be administered to patients whose oxygen saturation falls below the target saturation ranges (94-98% for most acutely ill patients and 88-92% for those at risk of type 2 respiratory failure with raised carbon dioxide level in the blood), and that those who administer oxygen therapy should monitor the patient and keep within those specified target saturation ranges.

But elsewhere in the world, delivery of high flow rates of oxygen for COPD patients (both pre-hospital and in-hospital) remained common.

 

In 2010,  a study (Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial)  was published in the BMJ that looked at the outcomes of patients with COPD who received high flow oxygen (compared to those who did not), and found their 30 day survival rate was worse.

 

I described the study in BMJ: Oxygen Delivery and COPD, and while the study was small, and subject to other limitations, they found:

• Titrated oxygen treatment reduces mortality, acidosis, and hypercarbia in patients with acute exacerbation of chronic obstructive pulmonary disease treated before arrival at hospital
• The risk of death was reduced by 78% by use of titrated oxygen rather than high flow oxygen, with a number needed to harm of 14
• These findings provide strong evidence that titrated oxygen treatment should be used for hypoxic or breathless patients with chronic obstructive pulmonary disease in prehospital settings

 

Fast forward a little over a year (January 2012), and in a blog called Oxygen Delivery & The Emergency Patient: Revisited, we looked at a retrospective study that appeared in the Archives of Internal Medicine that lent weight to the argument that when it comes to oxygen for emergency patients, less may be more.

Supplemental Oxygen Therapy in Medical Emergencies: More Harm Than Benefit?

Alexander D. Cornet, MD; Albertus J. Kooter, MD; Mike J. L. Peters, MD, PhD; Yvo M. Smulders, MD, PhD

Arch Intern Med. Published online January 9, 2012. doi:10.1001/archinternmed.2011.624

 

Smulders' team reviewed 18 previously conducted studies that looked at patient outcomes following oxygen treatment for common medical emergencies that included heart attacks, strokes, cardiac arrest, and COPD.

What they claim to have found is little or no evidence that high-dose oxygen improves survival, and weak evidence that it may even be detrimental. 

And not just for COPD patients.

 

The authors suggest that hyperoxia (excessive oxygen levels in the lungs, blood, or tissues) may cause hemodynamic changes that may actually increase myocardial ischemia (depriving heart muscle of oxygen) during a heart attack. They also propose that a relationship exists between hyperoxia and greater mortality and complications in non-cardiac emergencies as well.

 

All of which brings us to a new  Cochrane Review,  conducted by researchers at The University of Surrey and The City University London, that questions whether emergency oxygen is therapeutic for heart attack victims, and suggests it may even be detrimental.

 

First stop, the Cochrane review summary, then excerpts from the University of Surrey press release, after which I’ll return with a bit more.

 

Routine use of oxygen in people who have had a heart attack Updated

Cabello JB, Burls A, Emparanza JI, Bayliss S, Quinn T

Published Online:

August 21, 2013

(EXCERPT)

We found four randomised controlled trials that compared one group given oxygen to another group given air. These trials involved a total of 430 participants of whom 17 died. In that group, more than twice as many people known to have been given oxygen died compared to those known to have been given air. However, because the trials had few participants and few deaths, this result does not necessarily mean that giving oxygen increases the risk of death. The difference in numbers may have occurred simply by chance. Nonetheless, since the evidence suggests that oxygen may in fact be harmful, we think it is important to evaluate this widely-used treatment in a large trial as soon as possible, to make sure that current practice is not causing harm to people who have had a heart attack.

 

The Cochrane review process involves examining existing studies, eliminating those that do not meet certain strict standards, and then analyzing the results of those studies that they believe are well-mounted. While the intent is only to rely on `the best scientific evidence’, this process can winnow down the field of research to the point where there is insufficient data on which to make a determination.

 

And basically, that’s where this issue stands.  In their abstract, the author’s write::

 

There is no conclusive evidence from randomised controlled trials to support the routine use of inhaled oxygen in people with AMI. A definitive randomised controlled trial is urgently required, given the mismatch between trial evidence suggestive of possible harm from routine oxygen use and recommendations for its use in clinical practice guidelines.

In other words, we haven’t enough high quality studies to conclude – one way or the other – whether oxygen is helpful or detrimental to the heart attack victim.  Although I’d have put it in the lede, that assessment appears about 3/4ths of the way down the University of Surrey’s press release, in the following caveat:

 

Currently the number of participants involved is too low to enable conclusions about the effectiveness or harms of oxygen to be drawn.

 

Here are some excerpts from the press release. Follow the link to read it in its entirety.

 

No evidence to support giving oxygen to people having a heart attack, research shows

Monday 30 September 2013

Research shows that oxygen therapy following a heart attack may do more harm than good. 

For 100 years inhaled oxygen has been a standard treatment for those with a suspected or confirmed heart attack. The latest research, was led by academics from City University London and the University of Surrey, suggests that oxygen therapy may be doing more harm than good. 

More than seven million people – worldwide - die each year from coronary heart disease (CHD) and it is now the leading cause of death in the UK and US. A heart attack, or acute myocardial infarction, is often the first manifestation of CHD and a timely and appropriate intervention can make a significant difference to mortality rates. 

However, more than three years on from their first call for further research on the use of oxygen therapy, there are still wide variations in practice and the possibility that patients are either being harmed or deprived of benefit. 

Professor Tom Quinn, from the University of Surrey, comments: “While the changes to international guidelines for heart attack following our 2010 review are welcome, this new review suggests that we still do not have an evidence-based answer, based on an adequately powered and well conducted randomised trial, to confirm to clinicians and patients the role of oxygen therapy in heart attack treatment.  It is likely that a global collaboration will be required to deliver such a trial.” 

Professor Amanda Burls, from City University, said: “Our first review in 2010 on this topic called for more research to find out whether oxygen was useful or harmful. 

“While the review had a huge impact on practice, with many national and international guidelines changing from recommending routine use of oxygen to recommending it not to be used routinely, funding to run a trial to settle this important uncertainty has not yet been forthcoming.” 

(Continue . . . )

 

Amazingly, after a century of routine use, we don’t really know whether oxygen therapy is a help or a hindrance during a heart attack. The lack of well-mounted studies showing its efficacy isn’t enough to condemn it use, of course. 

 

But when coupled with other studies that suggest some degree of harm from oxygen is possible, and with the fate of millions of people each year in the balance, the need for better scientific evidence becomes glaringly obvious.

 

Stay tuned.

Study: Flu Vaccine May Reduce Heart Attack Risk

 

 

# 7592

 

In a perfect world, the conclusions drawn from medical research would always be unequivocal and we would be able to automatically accept their results as being the final word on the subject.

 

But as we’ve seen often in the past (When Studies Collide & When Studies Collide (Revisited)), no research methodology is perfect, all studies are subject to limitations, and it isn’t unusual to end up with conflicting results from different research teams.

 

While we would all like medicine to be based on treatments, drugs, and procedures proved – beyond a shadow of a doubt – to be safe and effective  . . . sometimes we must accept a lower burden of proof -the preponderance of evidence – instead.

 

All of which brings us to a new study out of Australia – published yesterday in the BMJ Journal Heart, that finds compelling – but not exactly conclusive – evidence that flu shots may reduce the risk of heart attacks.

 

If all of this sounds vaguely familiar, it’s because we’ve trod this ground before.

 

In 2010 we saw a study in the CMAJ: Flu Vaccinations Reduce Heart Attack Risk that found that those over the age of 40 who get a seasonal flu vaccine each year may reduce their risk of a heart attack by as much as 19%.

 

Almost immediately questions were raised over the way this study was conducted (see Vaccine/Heart Attack Study Questioned). The primary concern was these researchers only looked at heart attacks during `flu season’, without the control of looking at AMI risks year-round.

 

Last year, in Study: Influenza And Heart Attacks, we looked at a study appearing in the Journal of Infectious Diseases that suggested Influenza - and other acute respiratory infections - can act as a trigger for heart attacks.  There was an accompanying editorial called Increasing Evidence That Influenza Is a Trigger for Cardiovascular Disease published in the same issue.

 

In February of this year, in Another Study Links Heart Attacks & Influenza, we looked at a study from the University of Iowa that appeared in the January issue of the journal of Epidemiology and Infection linking spikes in AMIs (acute myocardial infarction) to influenza during the winter months, and also finds a similar spike in AMIs during the H1N1 pandemic wave of the fall of 2009.

 

Today’s study, which looked 559 patients over three flu seasons in Sydney, Australia, finds a 45% reduction in AMI risk among those who had received a flu vaccine.

 

They also found that those who had reported a recent respiratory infection were twice as likely to have a heart attack.  But the link between Influenza infection and an AMI was more tenuous.

 

Ischaemic heart disease, influenza and influenza vaccination: a prospective case control study

C Raina MacIntyre, Anita E Heywood, Pramesh Kovoor, Iman Ridda, Holly Seale, Timothy Tan, Zhanhai Gao, Anthea L Katelaris, Ho Wai Derrick Siu, Vincent Lo, Richard Lindley, Dominic E Dwyer

Published Online First 21 August 2013

Abstract

Background Abundant, indirect epidemiological evidence indicates that influenza contributes to all-cause mortality and cardiovascular hospitalisations with studies showing increases in acute myocardial infarction (AMI) and death during the influenza season.

Objective To investigate whether influenza is a significant and unrecognised underlying precipitant of AMI.

Design Case-control study.

Setting Tertiary referral hospital in Sydney, Australia, during 2008 to 2010.

Patients Cases were inpatients with AMI and controls were outpatients without AMI at a hospital in Sydney, Australia.

Main outcome measures Primary outcome was laboratory evidence of influenza. Secondary outcome was baseline self-reported acute respiratory tract infection.

Results Of 559 participants, 34/275 (12.4%) cases and 19/284 (6.7%) controls had influenza (OR 1.97, 95% CI 1.09 to 3.54); half were vaccinated. None were recognised as having influenza during their clinical encounter. After adjustment, influenza infection was no longer a significant predictor of recent AMI. However, influenza vaccination was significantly protective (OR 0.55, 95% CI 0.35 to 0.85), with a vaccine effectiveness of 45% (95% CI 15% to 65%).

Conclusions Recent influenza infection was an unrecognised comorbidity in almost 10% of hospital patients. Influenza did not predict AMI, but vaccination was significantly protective but underused. The potential population health impact of influenza vaccination, particularly in the age group 50–64 years, who are at risk for AMI but not targeted for vaccination, should be further explored. Our data should inform vaccination policy and cardiologists should be aware of missed opportunities to vaccinate individuals with ischaemic heart disease against influenza.

 

 

While these researchers found receiving the flu vaccine to provide statistically significant protection against a heart attack, a bit counter-intuitively, they were unable to directly link influenza to an increased risk of AMI.

 

They write:

 

While we showed a protective effect of influenza vaccination against AMI, we were unable to demonstrate a direct effect of influenza infection on AMI. This could reflect low statistical power, with laboratory-confirmed influenza being a much rarer event than vaccination, which showed significant association. Furthermore, the high vaccination rate in our participants likely reduced the risk of influenza and our ability to detect a difference between groups.

 

 

Teasing out the details of this study we have a report today in the Australian Academic & research news publication The Conversation, that includes the following reaction from other researchers.

 

2 August 2013, 9.04am AEST

Flu jab may halve heart attack risk: study

(EXCERPT)

Minimising risk

Julie Redfern, Senior Research Fellow, Cardiovascular Division at George Institute for Global Health welcomed the finding.

 

“Prevention of heart attacks and cardiovascular disease is a national health priority. Improving risk factors and implementing other simple measures aimed at preventing heart attacks and reducing the burden of disease are of great importance,” said Dr Redfern, who was not involved in the study.

 

“The potential of this study, after further research, that found a benefit of the flu vaccination on heart disease risk is important and could be one strategy that help minimise future heart risk.”

 

Garry Jennings, Director and CEO, Cardiologist at Baker IDI Heart and Diabetes Institute said the researchers had made a very interesting finding.

 

“It is not possible to say whether the flu vaccination was protective or whether people who have flu injections have other characteristics that lower their risk of heart attack. There is some support for the latter in that flu itself did not seem to increase the risk but people who had flu vaccination had lower risk,” said Dr Jennings, who was also not involved in the study.

 

“As the authors point out, this is cause for further investigation, particularly as there are some theoretical links related to inflammation that might have a role in the timing of a heart attack.”

 

 

While this study delivers something less than 100% proof that flu vaccines provide some protection against heart attacks, it does add incrementally to previous studies which have found links between respiratory infections, heart attacks, and `excess winter mortality’.

 

And if this link is valid, it makes sense that if you reduce the incidence of influenza (vaccines are usually about 50% effective) among those with coronary artery disease, you ought to reduce their rate of heart attacks.

 

But whether it makes sense or not, more research will be needed to know for sure. For more on this story, you may want to read Jason Gale’s report in Bloomberg News.

 

Flu Vaccine May Lower Heart Attack Risk, Researchers Find

By Jason Gale - Aug 21, 2013 6:30 PM ET

Another Study Links Heart Attacks & Influenza

 

# 6907

 

 

It is well established that death rates go up during the winter months, although the reasons behind these spikes in mortality are not entirely clear (or agreed upon). A few theories put forth include:

 

Colder temperatures, increased respiratory infections (including influenza & Pneumonia), over indulgence in food and alcohol, diminished activity levels, forgetting to take prescription medicines, and combined holiday stressors like shopping, running up debt, traveling, meal preparation, and the angst that comes from dysfunctional family gatherings . . . .

 

 

Nearly 15 years ago, a study looked at the rate of heart attacks in the United States, and found that Acute Myocardial Infarctions (AMIs) run as much 53% higher during the winter months than than during the summer.

 

Seasonal distribution of acute myocardial infarction in the second National Registry of Myocardial Infarction.

Spencer FA, Goldberg RJ, Becker RC, Gore JM.

 

While cold weather combined with strenuous physical activity (like clearing snow from sidewalks) has often been blamed for this spike, even in balmy Southern California, studies have shown a 33% increase in heart attacks over the holidays (see below).

 

When Throughout the Year Is Coronary Death Most Likely to Occur?

A 12-Year Population-Based Analysis of More Than 220 000 Cases

Robert A. Kloner, MD, PhD; W. Kenneth Poole, PhD; Rebecca L. Perritt, MS

 

Increasingly – but perhaps not conclusively - influenza and other respiratory infections have been linked to this seasonal increase in heart attacks.

 

Last October, in Study: Influenza And Heart Attacks, we looked at research that appeared in the Journal of Infectious Diseases that suggested Influenza - and other acute respiratory infections - can act as a trigger for heart attacks.

 

Influenza Infection and Risk of Acute Myocardial Infarction in England and Wales: A CALIBER Self-Controlled Case Series Study

Charlotte Warren-Gash, Andrew C. Hayward1, Harry Hemingway2, Spiros Denaxas2, Sara L. Thomas3, Adam D. Timmis5, Heather Whitaker6 and Liam Smeeth4

 

The same issue carried an editorial called Increasing Evidence That Influenza Is a Trigger for Cardiovascular Disease.

 

In 2010, in CMAJ: Flu Vaccinations Reduce Heart Attack Risk we saw what would turn out to be a controversial study (see Vaccine/Heart Attack Study Questioned) that strongly suggested that those over the age of 40 who get a seasonal flu vaccine each year may reduce their risk of a heart attack by as much as 19%.

 

So the idea that heart attacks may be linked to influenza infection is hardly new.

 

As winter brings many other elements into the equation  it has been difficult to isolate influenza as a major cause for the spike in AMIs during each winter.

 

Adding to our understanding of this issue, we have a study from the University of Iowa in the January issue of the journal of Epidemiology and Infection that links spikes in AMIs to influenza during the winter months, and also finds a similar spike in AMIs during the H1N1 pandemic wave of the fall of 2009.

 

Acute myocardial infarctions, strokes and influenza: seasonal and pandemic effects

E. D. FOSTER, J. E. CAVANAUGH, W. G. HAYNES, M. YANG, A. K. GERKE, F. TANG and P. M. POLGREEN

SUMMARY

The incidence of myocardial infarctions and influenza follow similar seasonal patterns. To determine if acute myocardial infarctions (AMIs) and ischaemic strokes are associated with influenza activity, we built time-series models using data from the Nationwide Inpatient Sample.

 

In these models, we used influenza activity to predict the incidence of AMI and ischaemic stroke. We fitted national models as well as models based on four geographical regions and five age groups.

 

Across all models, we found consistent significant associations between AMIs and influenza activity, but not between ischaemic strokes and influenza. Associations between influenza and AMI increased with age, were greatest in those aged >80 years, and were present in all geographical regions.

 

In addition, the natural experiment provided by the second wave of the influenza pandemic in 2009 provided further evidence of the relationship between influenza and AMI, because both series peaked in the same non-winter month.

 

The University of Iowa has a press release with more information, at the link below:

 

UI study suggests flu vaccine protects against heart attacks

Research focuses on older adults

Debra Venzke | 2013.02.04 | 07:02 AM

A new study from researchers at the University of Iowa suggests that the flu vaccine may provide protection against heart attacks in older adults, particularly those over age 80.

 

Scientists have long recognized that deaths due to influenza and deaths from other non-influenza-related diseases follow a similar seasonal pattern. This has lead researchers to suspect that acute infection caused by influenza may trigger events leading to heart attacks and strokes.

 

To determine if heart attacks and strokes are associated with influenza activity, the UI researchers built a set of time-series models using inpatient data from a national sample of more than 1,000 hospitals.

 

Across all models, the researchers found consistent significant associations between heart attacks and influenza activity. The study was published online Jan. 3 in the journal Epidemiology and Infection.

(Continue . . . )

 

The question of just how much protection the current flu shot technology provides to elderly persons is the subject of considerable debate as well (see NFID: The Challenges Of Influenza In Older Adults excerpts below)

 

 

From a 5-page brief, published in 2011, called: Understanding the Challenges and Opportunities in Protecting Older Adults from Influenza:

Although the elderly generally see less protection from the flu vaccine, older individuals may still mount a robust immune response. In populations 65 and older, the brief points out that:

• Hospitalization rates for influenza and pneumonia are lower in community-dwelling adults who received the seasonal influenza vaccine.
• Immunization is associated with reduced hospitalization of older patients for cardiac, respiratory, and cerebrovascular diseases.

While the goal of vaccinating the younger population is to prevent infection, the authors point out that:

• . . . the goal in older adults is to prevent severe illness, including exacerbation of underlying conditions, hospitalization, and mortality.

In other words, even if the vaccine doesn’t always prevent infection in the elderly, studies suggest that the vaccine may blunt the seriousness of the illness in those over 65.

 

 

As I reported on Friday in CDC FluView Week 4:

 

Influenza-related hospitalizations continue to be heavily skewed towards those over 65, reaching an 116.1 per 100,000 population, accounting for more than half of all hospitalizations.

 

 

And we are seeing levels of P&I (Pneumonia & Influenza) related mortality – predominately among the elderly – at rates unseen in a decade.

 

Which makes getting the current  flu vaccine – even if it is far less effective that we might desire -  better than going into influenza season having no protection at all.