The Ugly Side of Statins: Systemic Appraisal of the Contemporary Unknown Unknowns.


Story at-a-glance

  • A review of the published statin research revealed a categorical lack of evidence to support the use of statin therapy in primary prevention of heart attacks
  • Statins may actually increase cardiovascular risk in women, the young and people with diabetes
  • The cholesterol-lowering drugs are also linked to an increased risk of cataracts, memory impairment, diabetes, erectile dysfunction and over 300 adverse health effects
  • Lifestyle changes were far more effective, and safer, for primary heart attack prevention than statin drugs.
  • Statins

Statin cholesterol-lowering drugs are among the most widely prescribed drugs on the market, bringing in $20 billion a year.1 They are a top profit-maker for the pharmaceutical industry, in part due to relentless and highly successful direct-to-consumer advertising campaigns.

One in four Americans over the age of 45 now takes statins, typically for theprimary prevention of heart attacks and strokes. Traditionally, primary prevention usually involves healthy lifestyle choices that support heart health, things like eating right and exercising, yet here we have millions of Americans taking pills instead.

Has anyone unbiased stopped to find out if these drugs are really the best method for heart attack prevention? After all, as researchers noted in the Open Journal of Endocrine and Metabolic Diseases (OJEMD):2

“…naive indiscriminate acceptance of novel mainstream therapies is not always advisable and prudence is required in unearthing harmful, covert side effects.”

This is precisely the task that researchers from Ireland took on by completing an objective review of Pubmed, EM-BASE and Cochrane review databases.3 Their results speak volumes…

It is beginning to dawn on some clinicians that contemporary treatments are not only failing to impact on our most prevalent diseases, but they may be causing more damage than good. A perfect example of such an issue is the statin saga.”

The Evidence Is In: Lifestyle Trumps Statins for Primary Heart Attack Prevention

For a drug therapy that appears to offer little by way of primary prevention, the risks were alarming. For every 10,000 people taking a statin, there were:

  • 307 extra patients with cataracts
  • 23 additional patients with acute kidney failure
  • 74 extra patients with liver dysfunction

The landmark review revealed “a categorical lack of clinical evidence to support the use of statin therapy in primary prevention.” They also found that statins actually increase cardiovascular risk in women, the young and people with diabetes. The review also showed that statin therapy increased:

  • Muscle fatigabilty by 30% with more than 11% incidence of rhabdomyolysis (a life-threatening muscle condition) at high doses
  • Coronary artery and aortic calcification
  • Erectile dysfunction, which is 10 times more common in young men taking the lowest dose of statin.
  • Diabetes
  • Cancer

The researchers noted:

There is increased risk of diabetes mellitus, cataract formation, and erectile dysfunction in young statin users, all of which are alarming. Furthermore there is a significant increase in the risk of cancer and neurodegenerative disorders in the elderly plus an enhanced risk of a myriad of infectious diseases. All side effects are dose dependent and persist during treatment.

Primary prevention clinical results provoke the possibility of not only the lack of primary cardiovascular protection by statin therapy, but highlight the very real possibility of augmented cardiovascular risk in women, patients with diabetes mellitus and the young. Statins are associated with triple the risk of coronary artery and aortic calcification.

These findings on statins’ major adverse effects had been under-reported and the way in which they [were] withheld from the public, and even concealed, is a scientific farce.

 Cardiovascular primary prevention and regeneration programmes, through life style changes and abstaining from tobacco use have enhanced clinical efficacy and quality of life over any pharmaceutical or other conventional intervention.”

If You Take Statins, Your Vision Could Be at Risk

The featured review found an increased risk of cataracts with statin use, and this was supported by a new JAMA study,4 which further revealed that the risk of cataracts is increased among statin users, compared with non-users. As a main cause of low vision among the elderly, cataract is a clouding of your eye lens.

It has previously been hypothesized that statin antioxidant effects may slow the aging process of the lens, but the current study revealed that they, instead, raise cataract risk, again calling into question the usefulness of statins for primary prevention of heart attacks. The researchers concluded:

The risk-benefit ratio of statin use, specifically for primary prevention, should be carefully weighed, and further studies are warranted.”

Certain Statins May Impair Your Memory and May Even Lead to Amnesia

Still more research revealed that rats taking the statin Pravachol (pravastatin) had impaired learning, with lower abilities to perform simple learning and memory tasks.5 This isn’t exactly news, as in 2012, the US Food and Drug Administration (FDA) announced it would be requiring additional warning labels for statins, one of which warned that statins may increase the risk of memory loss and confusion. The warnings, particularly the one for memory loss, came as the result of anecdotal reports compiled over the previous year…

Interestingly, the animal study found no association between another statin drug, Lipitor, and impaired memory in the rats. But Dr. Duane Graveline, a medical doctor and former astronaut, has written an entire book on this very topic, titled Lipitor: Thief of Memory.

In my interview with him, Dr. Graveline shared his powerful story about how Lipitor caused him severe global transient amnesia, which is what brought him out of retirement to investigate statins. There have been thousands of cases of transient global amnesia and other types of cognitive damage associated with statin use, reported to the FDA’s MedWatch site. It is believed that statin drugs damage your brain by creating a cholesterol deficiency.

Insufficient cholesterol results in your brain not having the raw materials it needs to make biochemicals critical for memory and cognitive function, including coenzyme Q10 and dolichols, the latter of which carry the genetic instructions from your DNA to help create specific proteins in your body that are crucial for cognitive function, emotions and mood.

High Cholesterol Levels May Be Protective

Any discussion of statins would be incomplete without a discussion of cholesterol – the ‘villain’ that these drugs mercilessly lower. Many buy into the conventional belief that lower cholesterol equals a lower risk of heart disease, but this is not always the case. And, in fact, high cholesterol levels are indeed protective in some cases, whereas low cholesterol levels are very clearly linked to chronic disease. Writing in OJEMD, researchers explained:

“Cholesterol is crucial for energy, immunity, fat metabolism, leptin, thyroid hormone activity, liver related synthesis, stress intolerance, adrenal function, sex hormone syntheses and brain function. When prescribing HMGCoA reductase inhibitors [statins] one needs to be cognizant of the fact that the body had increased its’ cholesterol as a compensatory mechanism and investigate accordingly.

We seem to have fallen into the marketing trap and ignored the niggling side effects with regard to the HMGCoA reductase inhibitors. The only statin benefit that has actually been demonstrated is in middle-aged men with coronary heart disease. However, statins were not shown to best form of primary prevention.

… In actual fact, high cholesterol levels have been found to be protective in elderly and heart failure patients and hypo-cholestereamic [low cholesterol] patients had higher incidence of intra-cerebral bleeds, depression and cancer. … We are observing the revealing of the utmost medical tragedy of all time. It is unprecedented that the healthcare industry has inadvertently induced life-threatening nutrient deficiency in millions of otherwise healthy people. What is even more disparaging is that not only has there been a failure to report on these negative side-effects of statins, there has actually been active discouragement to publish any negative studies on statins.”

This is, in large part, why so many people are completely unaware that statin drugs have been directly linked to over 300 side effects,6 which include:

Cognitive loss Neuropathy Anemia
Acidosis Frequent fevers Cataracts
Sexual dysfunction An increase in cancer risk Pancreatic dysfunction
Immune system suppression Muscle problems, polyneuropathy (nerve damage in the hands and feet), and rhabdomyolysis, a serious degenerative muscle tissue condition Hepatic dysfunction. (Due to the potential increase in liver enzymes, patients must be monitored for normal liver function)

Ask Yourself – and Your informed Physician — if You Really Need to Be Taking Statins

I’ve long stated that the odds are very high — greater than 100 to 1 — that if you’re taking a statin, you may not even need it, ascholesterol is NOT the cause of heart disease. To further reinforce the importance of cholesterol, I want to remind you of the work of Dr. Stephanie Seneff, who works with the Weston A. Price Foundation.

One of her theories is that cholesterol combines with sulfur to form cholesterol sulfate, and that this cholesterol sulfate helps thin your blood by serving as a reservoir for the electron donations you receive when walking barefoot on the Earth (also called grounding). She believes that, via this blood-thinning mechanism, cholesterol sulfate may provide natural protection against heart disease.

In fact, she goes so far as to hypothesize that heart disease is likely the result of cholesterol deficiency — which of course is the complete opposite of the conventional view. So if your physician is urging you to check your total cholesterol, know that this test will tell you virtually nothing about your risk of heart disease, unless it is 330 or higher. HDL percentage is a far more potent indicator for heart disease risk. Here are the two ratios you should pay attention to:

  1. HDL/Total Cholesterol Ratio: Should ideally be above 24 percent. If below 10 percent, you have a significantly elevated risk for heart disease.
  2. Triglyceride/HDL Ratio: Should be below 2.

Additional risk factors for heart disease include:

  • Your fasting insulin level: Any meal or snack high in carbohydrates like fructose and refined grains generates a rapid rise in blood glucose and then insulin to compensate for the rise in blood sugar. The insulin released from eating too many carbs promotes fat production and makes it more difficult for your body to shed excess weight, and excess fat, particularly around your belly, is one of the major contributors to heart disease
  • Your fasting blood sugar level: Studies have shown that people with a fasting blood sugar level of 100-125 mg/dl had a nearly 300 percent increase higher risk of having coronary heart disease than people with a level below 79 mg/dl
  • Your iron level: Iron can be a very potent oxidative stress, so if you have excess iron levels you can damage your blood vessels and increase your risk of heart disease. Ideally, you should monitor your ferritin levels and make sure they are not much above 80 ng/ml. The simplest way to lower them if they are elevated is to donate your blood. If that is not possible you can have a therapeutic phlebotomy and that will effectively eliminate the excess iron from your body

Try This Instead for Primary Heart Attack Prevention

Make no mistake about it, statin drugs are some of the most side effect-ridden medications on the market, and they frequently do more harm than good. Of utmost importance, statins deplete your body of CoQ10, which accounts for many of its devastating results. Therefore, if you take a statin, you MUST take supplemental CoQ10, or better, the reduced form called ubiquinol. If you are interested in optimizing your cholesterol levels (which doesn’t necessarily mean lowering them) and lowering your risk of heart disease and heart attacks, there are natural strategies available for doing so.

  • Reduce, with the plan of eliminating, grains and sugars in your diet, replacing them with mostly whole, fresh vegetable carbs and healthy fats. Also try to consume a good portion of your food raw.
  • Make sure you are getting enough high-quality, animal-based omega-3 fats, such as krill oil.
  • Other heart-healthy foods include olive oil, coconut and coconut oil, organic raw dairy products and eggs, avocados, raw nuts and seeds, and organic grass-fed meats.
  • Optimize your vitamin D levels.
  • Exercise daily, especially with high-intensity interval training (HIIT) exercises.
  • Avoid smoking or drinking alcohol excessively.
  • Be sure to get plenty of good, restorative sleep.

Randomized Trial of Preventive Angioplasty in Myocardial Infarction.


Patients with acute ST-segment elevation myocardial infarction (STEMI) are effectively treated with emergency angioplasty, hereafter called percutaneous coronary intervention (PCI), to restore blood flow to the coronary artery that is judged to be causing the myocardial infarction (infarct artery, also known as culprit artery).1-5 These patients may have major stenoses in coronary arteries that were not responsible for the myocardial infarction,6 but the value of performing PCI in such arteries for the prevention of future cardiac events is not known.

Some physicians have taken the view that stenoses in noninfarct arteries may cause serious adverse cardiac events that could be avoided by performing preventive PCI during the initial procedure.7-12Others have suggested that medical therapy with antiplatelet, lipid-lowering, and blood-pressure–lowering drugs is sufficient and that the risks of preventive PCI outweigh the benefits.2-4,13-17

The aim of our single-blind, randomized study, called the Preventive Angioplasty in Acute Myocardial Infarction (PRAMI) trial, was to determine whether performing preventive PCI as part of the procedure to treat the infarct artery would reduce the combined incidence of death from cardiac causes, nonfatal myocardial infarction, or refractory angina.

DISCUSSION

The results of this trial show that in patients with acute STEMI, the use of preventive PCI to treat noninfarct coronary-artery stenoses immediately after PCI in the infarct artery conferred a substantial advantage over not performing this additional procedure. The combined rate of cardiac death, nonfatal myocardial infarction, or refractory angina was reduced by 65%, an absolute risk reduction of 14 percentage points over 23 months. The effect was similar in magnitude and remained highly significant when the analysis was limited to cardiac death and nonfatal myocardial infarction.

In this trial, all decisions regarding the treatment of patients, other than the random assignments to the two study groups, were left to the discretion of the clinicians involved. The rates of use of drug-eluting stents and medical therapy were similar in the two groups. In the group receiving no preventive PCI, ischemia testing was performed in about one third of patients: 44 tests in asymptomatic patients (usually ≤6 weeks after the myocardial infarction) and 37 tests in patients with chest pain. In the preventive-PCI group, ischemia testing was performed in about one sixth of patients: 8 tests in asymptomatic patients and 31 tests in patients with chest pain. Although such testing was not a prespecified trial outcome, these findings suggest that preventive PCI may lead to less ischemia testing and that when such testing is performed, it tends to be in patients with symptoms.

Although refractory angina is a more subjective outcome than myocardial infarction or cardiac death, it was included as a component of the primary outcome because it is a serious symptomatic condition that warrants prevention. We sought to reduce bias in the assessment of this outcome by requiring that the diagnosis be confirmed with objective evidence of ischemia. The benefit of preventive PCI was also evident when the less subjective outcomes of cardiac death and nonfatal myocardial infarction were considered alone.

We decided against using revascularization as a primary outcome, since subsequent revascularization procedures could be prompted by the identification of stenosis in a noninfarct artery in the group receiving no preventive PCI during the initial procedure. This factor would also tend to underestimate the effect of preventive PCI on primary-outcome events by reducing the treatment difference between the two study groups. However, revascularization was retained as a secondary outcome to record the number of subsequent procedures in each group.

In our study, 13 patients did not receive their assigned treatment. In the group receiving no preventive PCI, 2 patients underwent PCI in a noninfarct artery (1 for unknown reasons and 1 because the operator treated what turned out to be a noninfarct right coronary artery and then had to treat the infarct circumflex artery). In the preventive-PCI group, 11 patients underwent PCI only in the infarct artery because the preventive PCI could not be completed owing to insufficient time (because of competing emergency PCIs) in 3 patients, failure of the noninfarct-artery PCI in 5 patients, and other complications in 3 patients. These deviations from the assigned treatment mean that the intention-to-treat analysis, adopted to ensure comparability of the two study groups, will tend to underestimate the benefit of preventive PCI. However, the results of the as-treated analysis were consistent with those of the intention-to-treat analysis.

In two other randomized trials, investigators have specifically assessed the value of preventive PCI in patients with acute STEMI undergoing PCI in the infarct artery. In one study, 69 patients were randomly assigned (in a 3:1 ratio) to preventive PCI (52 patients) or no preventive PCI (17 patients).20 At 1 year, in the preventive-PCI group, there were nonsignificant reductions in the rates of repeat revascularization (17% and 35%, respectively) and cardiac death or myocardial infarction (4% and 6%, respectively). In the other trial, 214 patients were randomly assigned to one of three groups: no preventive PCI (84 patients), immediate preventive PCI (65 patients), and staged preventive PCI performed during a second procedure about 40 days later (65 patients).7 At 2.5 years, the rate of repeat revascularization was less frequent in the immediate– and staged–preventive PCI groups combined, as compared with the group receiving no preventive PCI (11% and 33%, respectively), and there was a nonsignificant decrease in the rate of cardiac death (5% and 12%, respectively). These studies were limited by a lack of statistical power and a reliance on repeat revascularization as an outcome, which, as indicated above, may be subject to bias. However, the results of these studies are consistent with those of our study.

Current guidelines on the management of STEMI recommend infarct-artery-only PCI in patients with multivessel disease, owing to a lack of evidence with respect to the value of preventive PCI.2-5 This uncertainty has led to variations in practice, with some cardiologists performing immediate preventive PCI in spite of the guidelines, some delaying preventive PCI until recovery from the acute episode, and others limiting the procedure to patients with recurrent symptoms or evidence of ischemia. The results of this trial help resolve the uncertainty by making clear that preventive PCI is a better strategy than restricting a further intervention to those patients with refractory angina or a subsequent myocardial infarction. However, our findings do not address the question of immediate versus delayed (staged) preventive PCI, which would need to be clarified in a separate trial.

Several questions remain. First, are the benefits of preventive PCI applicable to patients with non-STEMI?21 Such patients tend to be difficult to study because, unlike those with STEMI (in whom the infarct artery is invariably identifiable), there is often uncertainty over which artery is the culprit. Second, do the benefits extend to coronary-artery stenoses of less than 50%? There is uncertainty over the level of stenosis at which the risks of PCI outweigh the benefits. Third, would a physiological measure of blood flow, such as fractional flow reserve,22,23 offer an advantage over angiographic visual assessment in guiding preventive PCI? Further research is needed to answer these questions.

In conclusion, in this randomized trial, we found that in patients undergoing emergency infarct-artery PCI for acute STEMI, preventive PCI of stenoses in noninfarct arteries reduced the risk of subsequent adverse cardiovascular events, as compared with PCI limited to the infarct artery.

 

Source: NEJM

 

 

 

Living Longer With Obesity Increases Heart Risk.


We all know that carrying around extra weight increases the risk of heart disease, but the length of time a person has been toting that weight appears to be a factor as well. Children and adolescents who are obese — about 18% of the adolescent population right now — are in far more danger of developing heart disease than anyone ever considered.

Heart disease is the leading cause of death among men and women in the US, accounting for 600,000 deaths per year. Coronary heart disease, the most common form, develops when the arteries that supply the heart with blood, oxygen, and nutrients become damaged or diseased.

The usual cause is plaque, a combination of calcium, fat, cholesterol, and other substances. The accumulation of plaque, called atherosclerosis, is often the precursor to a heart attack or stroke.

Among those who were obese for over 20 years, 38 percent had calcification in the coronary arteries compared to 25 percent of those who never were obese. Higher rates of type 2 diabetes were also present in those who had been obese the longest.

Twenty-five years ago, at what we now know was the start of the obesity epidemic, researchers enrolled nearly 3,300 white and African-American adults between the ages of 18 and 30 in a study designed to look at the development of coronary artery disease in young adults. The participants were examined by a physician every two to five years and had CT scans at 15, 20, and 25 years into the study to detect calcification (hardening) in the coronary arteries.

The information collected on each participant included their body mass index, whether they smoked or not, cholesterol, blood pressure, physical activity level, and whether or not they developed type 2 diabetes.

How long a person had been overweight or obese was linked to accelerated atherosclerosis. Coronary artery calcification was discovered in nearly 28 percent of the participants. The length of time each person was obese, based on their physical exams over the years, correlated with the presence and the extent of blockage in the arteries. Among those who were obese for over 20 years, 38 percent had calcification in the coronary arteries compared to 25 percent of those who never were obese.

The risk of developing plaque increased by two to four percent for every year the young adults were obese, independent of all other factors measured on the participants. Those who had been obese the longest and who had abdominal obesity had increased odds of developing high blood pressure and elevated cholesterol and were more likely to be onmedications to control those conditions. Higher rates of type 2 diabetes were also present in those who had been obese the longest.

Overall, the study implies that the earlier one becomes obese, the more likely it is that major heart problems will develop by middle age. Given the fact that over the past thirty years the rate of obesity has doubled among children and tripled among adolescents, more of today’s children and teens are likely to experience coronary events as they reach mid-life.

People are becoming obese at younger ages than previous generations. The results of this study make clear that this will likely have significant implications on the incidence of heart disease in the future and underscore the need for programs aimed at tackling obesity among our children and teens.

Source: Journal of the American Medical Association.

 

Long-term obesity leads to greater heart risk, study finds.


Young adults who remain obese for two decades or more double their risk of developing a marker of heart disease in middle age, a study found.

Every year of obesity raises the risk of developing coronary artery calcification, a silent predictor of heart disease with mild to no symptoms, by 2 percent to 4 percent, according to research Wednesday in the Journal of the American Medical Association.

More than one third of U.S. adults ages 20 and older, and 17 percent of children and teenagers, are obese, according to the U.S. National Institutes of Health. About $147 billion a year is spent in the U.S. on obesity-related medical costs, according to a 2011 report. Wednesday’s study is the first to show that how long a person is obese can independently contribute to heart risk, said Jared Reis, the lead study author.

“What our study suggests is if we’re measuring only body mass index and waist circumference we may be underestimating the health risks of obesity by not measuring the duration,” Reis, an epidemiologist at the NIH’s National Heart, Lung, and Blood Institute in Bethesda, Md., said in a telephone interview.

Researchers looked at 3,275 adults ages 18 to 30 years who weren’t obese at the beginning of the study in the mid-1980s. Those in the study were given computed tomography scans to detect coronary artery calcification over 25 years. Their obesity and abdominal obesity also was measured.

The researchers found that about 38 percent of those who were obese for more than 20 years and 39 percent of those who had abdominal obesity for that time developed coronary artery calcification compared with 25 percent of those who never became obese and never developed abdominal obesity.

Those in the study who had obesity and abdominal obesity over two decades or more also had their coronary artery calcification progress in their heart.

Obesity is measured using body mass index, or BMI, a calculation of weight and height. For example, a 5-foot, 4-inch woman weighing 175 pounds (80 kilograms) has a BMI of 30. BMI of 30 or more is considered obese, while a BMI of 25 to 29.9 is considered overweight, according to the National Institutes of Health.

Reis said researchers will continue following those in the study to see how many actually develop clinical heart disease.

Source:         http://www.chicagotribune.com

Association Between Duration of Overall and Abdominal Obesity Beginning in Young Adulthood and Coronary Artery Calcification in Middle Age.


Importance  Younger individuals are experiencing a greater cumulative exposure to excess adiposity over their lifetime. However, few studies have determined the consequences of long-term obesity.

Objective  To examine whether the duration of overall and abdominal obesity was associated with the presence and 10-year progression of coronary artery calcification (CAC), a subclinical predictor of coronary heart disease.

Design, Setting, and Participants  Prospective study of 3275 white and black adults aged 18 to 30 years at baseline in 1985-1986 who did not initially have overall obesity (body mass index [BMI] ≥30) or abdominal obesity (men: waist circumference [WC] >102 cm; women: >88 cm) in the multicenter, community-based Coronary Artery Risk Development in Young Adults (CARDIA) study. Participants completed computed tomography scanning for the presence of CAC during the 15-, 20-, or 25-year follow-up examinations. Duration of overall and abdominal obesity was calculated using repeat measurements of BMI and WC, respectively, performed 2, 5, 7, 10, 15, 20, and 25 years after baseline.

Main Outcomes and Measures  Presence of CAC was measured by computed tomography at the year 15 (2000-2001), year 20 (2005-2006), or year 25 (2010-2011) follow-up examinations. Ten-year progression of CAC (2000-2001 to 2010-2011) was defined as incident CAC in 2010-2011 or an increase in CAC score of 20 Agatston units or greater.

Results  During follow-up, 40.4% and 41.0% developed overall and abdominal obesity, respectively. Rates of CAC per 1000 person-years were higher for those who experienced more than 20 years vs 0 years of overall obesity (16.0 vs 11.0, respectively) and abdominal obesity (16.7 vs 11.0). Approximately 25.2% and 27.7% of those with more than 20 years of overall and abdominal obesity, respectively, experienced progression of CAC vs 20.2% and 19.5% of those with 0 years. After adjustment for BMI or WC and potential confounders, the hazard ratios for CAC for each additional year of overall or abdominal obesity were 1.02 (95% CI, 1.01-1.03) and 1.03 (95% CI, 1.02-1.05), respectively. The adjusted odds ratios for CAC progression were 1.04 (95% CI, 1.01-1.06) and 1.04 (95% CI, 1.01-1.07), respectively. Associations were attenuated but largely persisted following additional adjustment for potential intermediate metabolic factors during follow-up.

Conclusions and Relevance  Longer duration of overall and abdominal obesity was associated with subclinical coronary heart disease and its progression through midlife independent of the degree of adiposity. Preventing or at least delaying the onset of obesity in young adulthood may lower the risk of developing atherosclerosis through middle age.

Source: JAMA

 

What causes coronary heart disease?


Coronary heart disease (CHD) is arguably the the UK’s biggest killer. CHD develops when the blood supply to the muscles and tissues of the heart becomes obstructed by the build-up of fatty materials inside the walls of the coronary arteries.

_67019810_heart122375065

What is coronary heart disease?

Your heart is a pump the size of a fist that sends oxygen-rich blood around your body. The blood travels to the organs of your body through blood vessels known as arteries, and returns to the heart through veins.

Your heart needs its own blood supply to keep working. Heart disease occurs when the arteries that carry this blood, known as coronary arteries, start to become blocked by a build-up of fatty deposits.

How common is CHD?

  • CHD causes round 74,000 deaths each year. That’s an average of 200 people every day
  • In the UK, there are an estimated 2.3 million people living with the condition
  • About one in six men and one in nine women die from the disease
  • Death rates are highest in Scotland and northern England
  • In the past couple of decades, deaths from CHD have nearly halved due to better treatments

Source: British Heart Foundation

The inner lining of the coronary arteries gradually becomes furred with a thick, porridge-like sludge of substances, known as plaques, and formed from cholesterol. This clogging-up process is known as atherosclerosis.

The plaques narrow the arteries and reduce the space through which blood can flow. They can also block nutrients being delivered to the artery walls, which means the arteries lose their elasticity. In turn, this can lead to high blood pressure, which also increases the risk of heart disease. This same process goes on in the arteries throughout the body, and can lead to high blood pressure which puts further strain on the heart.

If your arteries are partially blocked you can experience angina – severe chest pains that can spread across your upper body – as your heart struggles to keep beating on a restricted supply of oxygen. You are also at greater risk of a heart attack.

Some people have a higher risk of developing atherosclerosis due to genetic factors – one clue to this is a family history of heart disease in middle-age. Lifestyle factors that increase the risk include an unhealthy diet, lack of exercise, diabetes, high blood pressure and, most importantly, smoking.

However, in the past couple of decades deaths from coronary heart disease have nearly halved, thanks to better treatments.

What happens during a heart attack?

A heart attack happens when one of the coronary arteries becomes completely blocked. This usually happens when a plaque, which is already narrowing an artery, cracks or splits open. This triggers the formation of a blood clot around the plaque, and it is this blood clot that then completely blocks the artery.

With their supply of oxygen completely blocked, the heart muscle and tissue supplied by that artery start to die. Emergency medical intervention is needed to unblock the artery and restore blood flow. This may consist of treatment with drugs to dissolve the clot or thrombus, or a small operation done through the skin and blood vessels to open up the blocked artery.

The outcome of a heart attack hinges on the amount of the muscle that dies before it is corrected. The smaller the area affected, the greater the chance of survival and recovery.

While a heart attack will always cause some permanent damage, some areas may be able to recover if they are not deprived of blood for too long. The sooner a heart attack is diagnosed and treated, the greater the chance of recovery.

Other heart diseases

Other diseases that commonly affect the heart include:

  • Chronic heart failure – CHD is one of the main causes of heart failure. It affects around one million people in the UK, and many more have it but haven’t been formally diagnosed. Here, the heart doesn’t works effectively as a pump, and fluid gathers in the lower limbs and lungs. This causes a variety of symptoms and significantly reduces quality of life.
  • Infection – bacterial infections such as endocarditis are much rarer these days thanks to antibiotics, but can damage the valves of the heart as well as other tissues. Viral infections can damage the heart muscle leading to heart failure, or cause abnormal heart rhythms.
  • Congenital heart disease – a number of defects can develop in the heart as a baby grows in the womb. One example is a hole in the heart, also known as a septal defect. Congenital heart disease may cause abnormal blood flow and put excessive strain on the infant’s heart after it has been born.
  • Cardiomyopathy – a disease of the heart muscle that can occur for different reasons, including coronary heart disease, high blood pressure, viral infection, high alcohol intake and thyroid disease.

Source: BBC

 

High incidence of acute coronary occlusion in patients without protocol positive ST segment elevation referred to an open access primary angioplasty programme.


Abstract

Background Primary percutaneous coronary intervention (PPCI) programmes vary in admission criteria from open referral to acceptance of electrocardiogram (ECG) protocol positive patients only. Rigid criteria may result in some patients with acutely occluded coronary arteries not receiving timely reperfusion therapy.

Objective To compare the prevalence of acute coronary occlusion and, in these cases, single time point biomarker estimates of myocardial infarct size between patients presenting with protocol positive ECG changes and those presenting with less diagnostic changes in the primary angioplasty cohort of an open access PPCI programme.

Methods We retrospectively performed a single centre cross sectional analysis of consecutive patients receiving PPCI between January and August 2008. Cases were categorised according to presenting ECG—group A: protocol positive (ST segment elevation/left bundle branch block/posterior ST elevation myocardial infarction), group B: ST segment depression or T-wave inversion, or group C: minor ECG changes. Clinical characteristics, coronary flow grades and 12 h postprocedure troponin-I levels were reviewed.

Results During the study period there were 513 activations of the PPCI service, of which 390 underwent immediate angiography and 308 underwent PPCI. Of those undergoing PPCI, 221 (72%) were in group A, 41 (13%) in group B and 46 (15%) in group C. Prevalence of coronary occlusion was 75% in group A compared with 73% in group B and 63% in group C. Median 12 h postintervention troponin-I (25th–75th percentile) for those with coronary occlusion was significantly higher in group A patients; 28.9 μg/l (13.2–58.5) versus 18.1 μg/l (6.7–32.4) for group B (p=0.03); and 15.5 μg/l (3.8–22.0) for group C (p<0.001), suggesting greater infarct size in group A.

Conclusions A number of patients referred to an open access PPCI programme have protocol negative ECGs but myocardial infarction and acute coronary artery occlusion amenable to angioplasty.

Source: PMJ. BMJ

 


What causes coronary heart disease?

Coronary heart disease (CHD) is arguably the the UK’s biggest killer. CHD develops when the blood supply to the muscles and tissues of the heart becomes obstructed by the build-up of fatty materials inside the walls of the coronary arteries.

heart

What is coronary heart disease?

Your heart is a pump the size of a fist that sends oxygen-rich blood around your body. The blood travels to the organs of your body through blood vessels known as arteries, and returns to the heart through veins.

Your heart needs its own blood supply to keep working. Heart disease occurs when the arteries that carry this blood, known as coronary arteries, start to become blocked by a build-up of fatty deposits.

How common is CHD?

  • CHD causes round 74,000 deaths each year. That’s an average of 200 people every day
  • In the UK, there are an estimated 2.3 million people living with the condition
  • About one in six men and one in nine women die from the disease
  • Death rates are highest in Scotland and northern England
  • In the past couple of decades, deaths from CHD have nearly halved due to better treatments

Source: British Heart Foundation

The inner lining of the coronary arteries gradually becomes furred with a thick, porridge-like sludge of substances, known as plaques, and formed from cholesterol. This clogging-up process is known as atherosclerosis.

The plaques narrow the arteries and reduce the space through which blood can flow. They can also block nutrients being delivered to the artery walls, which means the arteries lose their elasticity. In turn, this can lead to high blood pressure, which also increases the risk of heart disease. This same process goes on in the arteries throughout the body, and can lead to high blood pressure which puts further strain on the heart.

If your arteries are partially blocked you can experience angina – severe chest pains that can spread across your upper body – as your heart struggles to keep beating on a restricted supply of oxygen. You are also at greater risk of a heart attack.

Some people have a higher risk of developing atherosclerosis due to genetic factors – one clue to this is a family history of heart disease in middle-age. Lifestyle factors that increase the risk include an unhealthy diet, lack of exercise, diabetes, high blood pressure and, most importantly, smoking.

However, in the past couple of decades deaths from coronary heart disease have nearly halved, thanks to better treatments.

What happens during a heart attack?

A heart attack happens when one of the coronary arteries becomes completely blocked. This usually happens when a plaque, which is already narrowing an artery, cracks or splits open. This triggers the formation of a blood clot around the plaque, and it is this blood clot that then completely blocks the artery.

With their supply of oxygen completely blocked, the heart muscle and tissue supplied by that artery start to die. Emergency medical intervention is needed to unblock the artery and restore blood flow. This may consist of treatment with drugs to dissolve the clot or thrombus, or a small operation done through the skin and blood vessels to open up the blocked artery.

The outcome of a heart attack hinges on the amount of the muscle that dies before it is corrected. The smaller the area affected, the greater the chance of survival and recovery.

While a heart attack will always cause some permanent damage, some areas may be able to recover if they are not deprived of blood for too long. The sooner a heart attack is diagnosed and treated, the greater the chance of recovery.

Other heart diseases

Other diseases that commonly affect the heart include:

  • Chronic heart failure – CHD is one of the main causes of heart failure. It affects around one million people in the UK, and many more have it but haven’t been formally diagnosed. Here, the heart doesn’t works effectively as a pump, and fluid gathers in the lower limbs and lungs. This causes a variety of symptoms and significantly reduces quality of life.
  • Infection – bacterial infections such as endocarditis are much rarer these days thanks to antibiotics, but can damage the valves of the heart as well as other tissues. Viral infections can damage the heart muscle leading to heart failure, or cause abnormal heart rhythms.
  • Congenital heart disease – a number of defects can develop in the heart as a baby grows in the womb. One example is a hole in the heart, also known as a septal defect. Congenital heart disease may cause abnormal blood flow and put excessive strain on the infant’s heart after it has been born.
  • Cardiomyopathy – a disease of the heart muscle that can occur for different reasons, including coronary heart disease, high blood pressure, viral infection, high alcohol intake and thyroid disease.

Source: BBC

 

What causes coronary heart disease?


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Coronary heart disease (CHD) is arguably the the UK’s biggest killer. CHD develops when the blood supply to the muscles and tissues of the heart becomes obstructed by the build-up of fatty materials inside the walls of the coronary arteries.

What is coronary heart disease?

Your heart is a pump the size of a fist that sends oxygen-rich blood around your body. The blood travels to the organs of your body through blood vessels known as arteries, and returns to the heart through veins.

Your heart needs its own blood supply to keep working. Heart disease occurs when the arteries that carry this blood, known as coronary arteries, start to become blocked by a build-up of fatty deposits.

How common is CHD?

  • CHD causes round 74,000 deaths each year. That’s an average of 200 people every day
  • In the UK, there are an estimated 2.3 million people living with the condition
  • About one in six men and one in nine women die from the disease
  • Death rates are highest in Scotland and northern England
  • In the past couple of decades, deaths from CHD have nearly halved due to better treatments

Source: British Heart Foundation

The inner lining of the coronary arteries gradually becomes furred with a thick, porridge-like sludge of substances, known as plaques, and formed from cholesterol. This clogging-up process is known as atherosclerosis.

The plaques narrow the arteries and reduce the space through which blood can flow. They can also block nutrients being delivered to the artery walls, which means the arteries lose their elasticity. In turn, this can lead to high blood pressure, which also increases the risk of heart disease. This same process goes on in the arteries throughout the body, and can lead to high blood pressure which puts further strain on the heart.

If your arteries are partially blocked you can experience angina – severe chest pains that can spread across your upper body – as your heart struggles to keep beating on a restricted supply of oxygen. You are also at greater risk of a heart attack.

Some people have a higher risk of developing atherosclerosis due to genetic factors – one clue to this is a family history of heart disease in middle-age. Lifestyle factors that increase the risk include an unhealthy diet, lack of exercise, diabetes, high blood pressure and, most importantly, smoking.

However, in the past couple of decades deaths from coronary heart disease have nearly halved, thanks to better treatments.

What happens during a heart attack?

A heart attack happens when one of the coronary arteries becomes completely blocked. This usually happens when a plaque, which is already narrowing an artery, cracks or splits open. This triggers the formation of a blood clot around the plaque, and it is this blood clot that then completely blocks the artery.

With their supply of oxygen completely blocked, the heart muscle and tissue supplied by that artery start to die. Emergency medical intervention is needed to unblock the artery and restore blood flow. This may consist of treatment with drugs to dissolve the clot or thrombus, or a small operation done through the skin and blood vessels to open up the blocked artery.

The outcome of a heart attack hinges on the amount of the muscle that dies before it is corrected. The smaller the area affected, the greater the chance of survival and recovery.

While a heart attack will always cause some permanent damage, some areas may be able to recover if they are not deprived of blood for too long. The sooner a heart attack is diagnosed and treated, the greater the chance of recovery.

Other heart diseases

Other diseases that commonly affect the heart include:

  • Chronic heart failure – CHD is one of the main causes of heart failure. It affects around one million people in the UK, and many more have it but haven’t been formally diagnosed. Here, the heart doesn’t works effectively as a pump, and fluid gathers in the lower limbs and lungs. This causes a variety of symptoms and significantly reduces quality of life.
  • Infection – bacterial infections such as endocarditis are much rarer these days thanks to antibiotics, but can damage the valves of the heart as well as other tissues. Viral infections can damage the heart muscle leading to heart failure, or cause abnormal heart rhythms.
  • Congenital heart disease – a number of defects can develop in the heart as a baby grows in the womb. One example is a hole in the heart, also known as a septal defect. Congenital heart disease may cause abnormal blood flow and put excessive strain on the infant’s heart after it has been born.
  • Cardiomyopathy – a disease of the heart muscle that can occur for different reasons, including coronary heart disease, high blood pressure, viral infection, high alcohol intake and thyroid disease.

Source: BBC

 

 

Coronary artery calcium score prediction of all cause mortality and cardiovascular events in people with type 2 diabetes: systematic review and meta-analysis


 

Objective To investigate the association of coronary artery calcium score with all cause mortality and cardiovascular events in people with type 2 diabetes.

Design Systematic review and meta-analysis of observational studies.

Data sources Studies were identified from Embase, PubMed, and abstracts from the 2011 and 2012 annual meetings of the American Diabetes Association, European Association for the Study of Diabetes, American College of Cardiology, and American Heart Association (2011).

Eligibility criteria Prospective studies that evaluated baseline coronary artery calcium score in people with type 2 diabetes and subsequent all cause mortality or cardiovascular events (fatal and non-fatal).

Data extraction Two independent reviewers extracted the data. The predictive value of the coronary artery calcium score was assessed by random effects model.

Results Eight studies were included (n=6521; 802 events; mean follow-up 5.18 years). The relative risk for all cause mortality or cardiovascular events, or both comparing a total coronary artery calcium score of ≥10 with a score of <10 was 5.47 (95% confidence interval 2.59 to 11.53; I2=82.4%, P<0.001). The overall sensitivity of a total coronary artery calcium score of ≥10 for this composite outcome was 94% (95% confidence interval 89% to 96%), with a specificity of 34% (24% to 44%). The positive and negative likelihood ratios were 1.41 (95% confidence interval 1.20 to 1.66) and 0.18 (0.10 to 0.30), respectively. For people with a coronary artery calcium score of <10, the post-test probability of the composite outcome was about 1.8%, representing a 6.8-fold reduction from the pretest probability. Four studies evaluated cardiovascular events as the outcome (n=1805; 351 events). The relative risk for cardiovascular events comparing a total coronary artery calcium score of ≥10 with a score of <10 was 9.22 (2.73 to 31.07; I2=76.7%, P=0.005). The positive and negative likelihood ratios were 1.67 (1.30 to 2.17) and 0.11 (0.04 to 0.29), respectively.

Conclusion In people with type 2 diabetes, a coronary artery calcium score of ≥10 predicts all cause mortality or cardiovascular events, or both, and cardiovascular events alone, with high sensitivity but low specificity. Clinically, the finding of a coronary artery calcium score of <10 may facilitate risk stratification by enabling the identification of people at low risk within this high risk population.

Discussion

In people with type 2 diabetes, the presence of a coronary artery calcium score of ≥10 predicts both all cause mortality and cardiovascular events as well as cardiovascular events alone, with high sensitivity but low specificity. The negative likelihood ratio of the coronary artery calcium score for these outcomes was strikingly low (0.18 for all cause mortality and cardiovascular events, and 0.11 for cardiovascular events). Indeed, our evaluation of risk estimates through the Bayes normogram suggests that the coronary artery calcium score may be especially helpful in clinical practice when it is below 10.

Our meta-analyses showed that the coronary artery calcium score might have a role in predicting events in people with type 2 diabetes. The findings of an increased relative risk for all cause mortality and cardiovascular events and cardiovascular events alone were consistent. The exploratory analysis of heterogeneity identified the variables associated with higher variance between studies, especially for cardiovascular events alone (where the sensitivity analysis eliminated the heterogeneity). We used the likelihood ratio as an alternative statistic because of its clinical applicability. Interestingly, we found a low negative likelihood ratio, in the range (that is, 0.1) that Deeks and Altman have previously suggested as providing strong evidence for ruling out the occurrence of an outcome in most circumstances.37

When evaluating a predictor of adverse outcomes, it is recognised that a useful predictor should have a favourable risk-benefit ratio, reasonable cost, acceptability, and convenience. In addition, to make screening worthwhile an effective treatment should be available, and this treatment should not be equally effective in everyone.38 In this context, screening using the coronary artery calcium score is a convenient and non-invasive test, although it involves exposure to ionising radiation of about 1 millisieverts (which is comparable to screening mammography).39 No formal cost effectiveness analyses have been done on the coronary artery calcium score in people with type 2 diabetes integrating risk, benefits, and cost; however, the current findings raise the possibility that screening using the coronary artery calcium score may be cost effective in some subgroups of people with diabetes. Moreover, a previous report showed that patient awareness of an abnormal score was associated with increased adherence to aspirin use and lifestyle changes,40 suggesting that, besides risk stratification, the coronary artery calcium score might help to support behavioural modification.

The American Heart Association has supported the use of the coronary artery calcium score quantification in people at intermediate risk to improve risk assessment (class IIb recommendation).41 Conversely, the American Diabetes Association does not recommend its routine use in people with type 2 diabetes because the overall balance of risk, benefits, and cost of such an approach in people without symptoms remains controversial.1 In light of the lack of previous evidence to support the routine use of the coronary artery calcium score as a screening test in people with type 2 diabetes, we feel that the current meta-analysis is much needed and holds implications for the design of future studies. In particular, the finding of such a low likelihood ratio suggests that a coronary artery calcium score of <10 might help with risk stratification of people with type 2 diabetes and potentially would change prevention strategies in those people. In fact, it has been suggested that the coronary artery calcium score may help to identify people with diabetes who may benefit from aspirin therapy among those without a clear indication based on current guidelines.13 Most importantly, if we consider that the prevalence of a coronary artery calcium score of <10 was 28.5% in our study population, the current findings might have an important impact on clinical care. Indeed, considering the worldwide prevalence of 346 million cases of type 2 diabetes,42 these data suggest that about 86.5 million people with type 2 diabetes would have a coronary artery calcium score of <10 and hence a low risk of cardiovascular events. In addition, a score of <10 has been observed in a significant proportion of people with diabetes at intermediate risk on pretest assessment, a subgroup of people who would most benefit from the coronary artery calcium score test.13 33 In this way, screening using the coronary artery calcium score may facilitate clinical risk stratification by identifying a sizeable subgroup of people at low risk within the high risk population of people with diabetes.

The concept of a low risk subgroup within the population of people with diabetes has been demonstrated in a previous report that showed a similar risk of all cause mortality between people with and without diabetes who had no coronary artery calcium score at baseline (survival 98.8% v 99.4% over five years, P=0.49).30 These data reinforce the results of our meta-analysis, in which a coronary artery calcium score of <10 was indicative of low risk for future events in people with diabetes. In addition, in the same way that the coronary artery calcium score adds to current predictive scores in the general population,6 these data raise the possibility that incorporation of coronary artery calcium score into existing risk scores for people with diabetes might improve risk prediction and hence warrants further investigation.

Limitations of this review

A limitation of our meta-analysis is that an analysis of additional risk stratification beyond current available risk scores for people with type 2 diabetes could not be performed owing to the absence of such studies. Secondly, most studies did not take into consideration the use of drugs (that is, aspirin and lipid lowering drugs) that could interfere with the estimates of event rate prediction based on the coronary artery calcium score. Nevertheless, as all studies were performed after 2004, we believe that the people were possibly treated similarly based on current clinical practice recommendations. Thirdly, only three studies reported baseline glycated haemoglobin A1c and duration of diabetes. However, although these covariates could not be included in metaregression analyses, our models were able to identify the studies that better explained the variance between studies. Of note, although most studies measured the coronary artery calcium score using the same technique, differences in the protocol for obtaining the scores could also have contributed to the variance between studies. Finally, we recognise that publication bias and the quality limitations of individual studies may still be relevant despite our best efforts to conduct a comprehensive search and the lack of statistical evidence of bias. The subjective nature of the Newcastle-Ottawa scale by which the quality of studies was assessed should also be noted.

Our meta-analysis strongly suggests that the coronary artery calcium score warrants further investigation as a prediction tool in people with type 2 diabetes. In particular, randomised controlled trials evaluating the impact of screening using the coronary artery calcium score on mortality are needed. Another point to consider in future studies is that atherosclerosis is a dynamic process, as shown by studies documenting both progression and regression of plaque.43 44 45 Glucose levels are an independent risk factor for progression of coronary artery calcium score,46 and people with type 2 diabetes have been shown to have a higher rate of progression than those without diabetes.47 Thus, the optimal frequency of screening using the coronary artery calcium score also needs to be established.

Conclusion

The coronary artery calcium score predicts all cause mortality and cardiovascular events and cardiovascular events alone in people with type 2 diabetes. People with a coronary artery calcium score of <10 were 6.8 times less likely to have cardiovascular event. Taken together, our meta-analysis strongly suggests the need for further investigation of the utility of using the coronary artery calcium score, particularly because of the implications that a negative screening test may hold for clinical risk stratification and preventive management in this population.

What is already known on this topic

  • The coronary artery calcium (CAC) score has been shown to predict the risk for cardiovascular events and facilitate reclassification of people from intermediate to low or high risk in large prospective studies of the general population
  • However, most of these studies excluded people with diabetes
  • The role of the CAC score in people with type 2 diabetes is unclear and given the broad range of cardiovascular risk observed in people with diabetes, this population warrants focused investigation on the predictive capacity of the CAC score
  • A CAC score of ≥10 predicted all cause mortality or cardiovascular events, or both compared with a score of <10, with high sensitivity but low specificity
  • For people with a CAC score of <10, the post-test probability of all cause mortality or cardiovascular events was reduced by 6.8-fold from their pretest probability
  • In people with diabetes, the finding of a CAC score of <10 may facilitate risk stratification by enabling the identification of low risk people within this otherwise high risk population

What this study adds

Source: BMJ