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ALMOST half of people who have been hospitalised with a heart attack are not receiving the intensive lipid-lowering therapy that could help to reduce their high risk of a further event, according to Australian research, and women, particularly, are being undertreated.
In a study published online by the MJA, 1565 of 3441 patients (45%) were not receiving intensive lipid-lowering therapy, defined as treatment with atorvastatin (≥ 40 mg/day), rosuvastatin (≥ 20 mg/day), or simvastatin (≥ 80 mg/day), with or without ezetimibe 6 or 12 months after hospitalisation for confirmed acute coronary syndrome.
The researchers analysed patients enrolled in the CONCORDANCE (Cooperative National Registry of Acute Coronary care, Guideline Adherence and Clinical Events) registry between January 2015 to May 2016. They found that, 6 or 12 months after discharge, 826 patients (24%) were receiving some form of lipid-lowering therapy other than the recommended intensive therapy, and 739 patients (22%) were receiving no lipid-lowering therapy at all.
The key predictors of not receiving intensive lipid-lowering therapy were not being prescribed treatment prior to their hospital admission (odds ratio [OR], 1.53) or discharge (adjusted OR [aOR], 7.24), being a woman (aOR, 1.20), and not being referred for cardiac rehabilitation (aOR, 1.39).
The researchers found that almost one in five patients were not prescribed high intensity lipid-lowering therapy at the time of discharge, and unmeasured hospital factors accounted for 17% of the variation in the likelihood of patients receiving intensive lipid-lowering therapy at follow-up.
They also found that patients who were managed medically in hospital (not revascularised; aOR, 1.54) or underwent coronary artery bypass grafting (aOR, 1.55) were less likely to be receiving intensive lipid-lowering therapy at follow-up than those with a percutaneous coronary intervention.
Professor Stephen Nicholls, Heart Health Theme Leader at the South Australian Health and Medical Research Institute and Professor of Cardiology at the University of Adelaide, said the findings were disappointing, but not surprising.
“We know from the large clinical trials that aggressively lowering [low-density lipoprotein] cholesterol with the highest dose of the statins is the standard of care for [high-risk] patients like the ones in the MJA study cohort,” he told MJA InSight.
“Yet, not only are there patients who go home without highest doses of the statin, many patients end up on either low dose statin or no statin 12 months down the track,” Professor Nicholls said.
“That worries all of us because the people at highest risk of having a heart attack are people who have had one before. We should be doing as much as we can to lower their likelihood of having another event, which may be potentially fatal.”
He said a further “striking” message in the research was that being a woman was a predictor of not being on intensive lipid-lowering therapy.
“The data very clearly show that women benefit just as much as men do from these drugs and … it worries me greatly when I see reports like this that suggest, yet again, that women are being undertreated. Not only do we have a lot to do in general [regarding adherence to secondary prevention measures], we are clearly not winning the messaging about treating women aggressively.”
In an exclusive MJA InSight podcast, lead researcher on the MJA article, Professor David Brieger, Professor of Cardiology at the University of Sydney’s Concord Clinical School, said despite being at high risk of a recurrent event, people tended to think they were “fine” after being hospitalised and treated for acute coronary syndrome.
“People … tend to feel better because their symptoms have gone,” Professor Brieger said. “But we know that a significant proportion will re-present with either further heart attacks or heart failure or, further chest pain or strokes. And those presentations make up about 30–40% of the acute presentations we see.”
Professor Gerald Watts, Professor of Cardiometabolic Medicine at the University of Western Australia and a consultant physician at Royal Perth Hospital, said the findings reflected the experience internationally, as demonstrated in the EUROASPIRE surveys.
“Despite all the hype about genetic testing and precision medicine, the basic adherence to therapies that are proven to prevent recurrent events – lowering cholesterol, controlling diabetes, stopping smoking, controlling blood pressure – is still not getting to the people who need it most,” he said.
“There is a lot of work to be done in trying to get these simple treatments fully implemented for these very high risk individuals.”
Professor Watts said effort needed to be invested across all facets of care, at the policy level, organisational level, doctor level, and patient level.
“There are physician factors here – there is less impetus to control risk factors than it is to do more procedures in cardiology, and a higher threshold to focus on secondary prevention,” he said.
“Secondary prevention can be carried out effectively if there is an integrated system between the hospital and primary care – you can’t expect this to be the responsibility of just a single [sector]. The volume of patients is so large, [secondary prevention initiatives] have to involve, in large measure, the primary care sector and the community.”
Professor Brieger said statins had had some “bad press” in recent years, and while this may be partly justified for use in primary prevention in low risk patients, the evidence of benefit was unequivocal in high risk patients.
“The concerns that we have had as clinicians is that the fallout from this bad press was that patients who have had previous events – and were, by definition, at very high risk of having further events – were also stopping their therapies,” he said, adding that these findings had confirmed anecdotal reports of patients ceasing statin therapy.
Professor Nicholls agreed, adding that the number of media reports of potential adverse effects with statins “grossly outweighed” the number of articles about the benefits of statins.
Professor Nicholls said the study underlined the key role that cardiac rehabilitation could play in improving adherence with lipid-lowering therapies.
“Cardiac rehabilitation plays an important role because a patient is in hospital for [up to] 4 days after a heart attack – there’s a lot happening, lots of people talking, and they are not necessarily taking it all in,” he said. “Cardiac rehabilitation classes are critical because it’s a great opportunity for patients to sit down with rehabilitation nurses who can demystify the whole [event] and explain what the patient needs to do to prevent ending up back in hospital or worse.”
Professor Nicholls said web-based approaches and text messaging initiatives were being explored as possible ways to increase accessibility of cardiac rehabilitation services.
I have been on statins since my AMI 10 year ago. Lipids normal at the time, and no demonstrable risk factors. LAD stent The statins certainly are not without side effects. Muscle pain and fatigue being the most pronounced. Have tried all the available statin groups, repeatedly tried off with resolution of Sx, re challenged and Sx back. Atorvastatin esp was unbearable even at 5 mg. Co Q 10 of dubious help.
Any cardiologist who says that it’s all media hype is not really listening to their patients. Nevertheless I’m still on the statins with a satisfactory lipid profile.
Lower and lower is not better. What about those born with the inborn error of metabolism and cannot produce any LDL at all. They have severe peripheral neuropathies and die young from this.
Cannot treat patients problems in isolation. Patients aren’t just hearts.
Hang on a bit! What are you calling “intensive lipid management”?
Are not the NHF guidelines for lipids post coronary disease recommending an LDL under 1.8? Have the goalposts been shifted when we weren’t looking?
If LDL can be lowered beneath 1.8 with less than maximal statins why not follow the principle of using the least amount of medication to achieve the required outcome?
In the real world of secondary prevention/chronic disease management i.e. General Practice, I find patients are upset that they have been slammed onto maximum dose of statin without individualising their dose, which risks compliance. In GP-land, I know we can do the job with a bit more finesse, with our patients remaining onside. Why not support that?
So if there is a good reason for maximum statins vs. titrated statin/combo therapy to achieve recommended target, please update the NHF recommendations.
Is there a PsychoCardioMetabolic Doctor in the house???? Medicine is grossly off-target with both cardiac diagnosis [i.e. WHO gets the AMI?}, and is very lucky indeed, that statins do MUCH more than lower LDL–their much-discussed “pleiotropic” effects on vascular inflammation and thrombosis may be much more important in their overall benefit profile.
Guys, it hurts to have to say this, but I suspect that MOST AMI cases have the above PsychoCardioMetabolic Syndrome. Smoking doubles the risk, and confused folks who cannot simplify do trot out a list of risk factors–BP, diabetes, high cholesterol, family history etc..
But dietary FAT does NOT affect risk at all, except when MUM eats it: take a look at the old Metabolic Syndrome, before Cardio- and Psycho- had to be added.
1. Fatty maternal diet [at least 25% of our pregnancies] causes mild placental inflammation, which allows maternal cortisol to breach the foeto-placental enzymatic barrier. Her cortisol programmes lifelong Anxiety Disorder in the foetal brain at about 25-30 weeks gestation, by epigenetically suppressing the foetus’s negative feedback signals from its own adrenal cortisol: the pub’s HPA axis [AND sympathetic nerves] are activated for life.
2. Mum’s yummy butter, cream, cheese, ice-cream, Maltesers, dairy milk chocolate, cakes and pastries, fatty sausages, salami, mortadella, cooking fat and super-tasty, super-greasy chicken–irresistible!!–mean she has an anxious child, with all the proliferating consequences of too much cortisol and a hyped-up sympathetic nervous system.
3. Which are insulin resistance, central fat, hypertension and dyslipidaemia [NOT much rise in total cholesterol, unless fat is eaten by the anxious offspring]. Gerald Reaven, in 1988, called this strange combination the Deadly Quartet–then it was called Syndrome X [“X” means we dunno what causes it], then [with a hint of science creeping into medicine] Metabolic Syndrome, because it looks like pre-diabetes, guys!
4. Years later, somebody realised that lots of Met S folks were dropping dead–as old-fashioned type 2 diabetics were long known to do. So the Cardio- got added. Next, with heart in the picture, one or two rare guys looking at the problem fancied there might be a bit of “stress”–they may have got that from the heart disease/depression literature, or even from the old stuff from Friedman, about stress and heart disease, Type A guys dropping dead etc.. Met S on WIKI gets a comment about “stress”, but that’s rare.
5. Medicine needs an Equation, and here it is:
Lay the Deadly Quartet out on a table, in a square shape. Now, add a second square above the first, to incorporate 4 more recent additions to Met S: thrombotic state, low-grade inflammation, raised urate, and microalbuminuria. We now have Metabolic Syndrome Cubed–MS[3]!!
And the whole thing is simply prenatal-acquired Anxiety, so we now have Medicine’s First-Ever SCIENTIFIC EQUATION: A=MS[3]!!! Einstein (E=MC[2]) eat your heart out!! And when we look more deeply at all the nasty effects of chronic cortisol and sympathetic overactivity, on the Top Ten Tissues of the once-healthy human body, we can expand or modify my Deadly Equation; e.g. let’s try A=HAD-IT, to cover Heart/Anxiety/Diabetes–Insidious Trio. Not to mention stress-related food cravings, drug and alcohol, heart failure, cognitive decline, auto-immunity, osteoporosis, thin skin/hair/nails, Parkinson’s etc..
Many years ago, a very smart US lipid researcher, Dr Margaret Albrink, stressed the importance of TRIGLYCERIDES as a far more common risk factor than raised cholesterol, for heart risk. She was TOTALLY ignored, as was LOW HDL, that came in later. Feed fat to a pregnant rat, and the offspring have–guess what!–RAISED TRIGS and LOW HDL!!! Check on PubMed [poston l and hdl, or poston l and triglycerides, and you should find Prof Lucilla Poston’s brilliant London study from years ago.
Fat-fed monkey and mouse dams also produce ANXIOUS offspring, complete with LOW-GRADE INFLAMMATION, guys!! Syndrome X turns to to be SYNDROME FATTY MATERNAL DIET.
What to do about this, then? Well, the best and brightest remedy for Anxiety–and therefore for MS[3] or HAD-IT is surely the seed sugar myo-inositol–it not only reverses anxiety quickly [by blocking strategic 5-HT-2 receptors, so calming both cortisol and the sympathetic–with all the Deadly Quartet-cum-Octet death-dealing features wiped out in days. It also induces the expression of over 500 cytoptotective anti-ageing genes [by blocking IGF-1 signalling]–including enhanced energy production and antioxidant levels in all tissues, including HEART.
Inositol was in the grains, nuts and legumes used in the Mediterranean diet-based Lyon Heart Study, run by Dr Michel De Lorgeril many years ago. Check this out–although he used 100s, not 1000s of subjects, I think he did select cases who HAD a history of heart or stroke, i.e.. high-risk cases.
He claimed a whopping 72% reduction in risk in the first year, which moderated later to about 55%. Note that inositol’s hit on serotonin 2A receptors means a direct anti-PLATELET action, in addition to calming an anxious brain. A quietened central sympathetic also means less hsCRP and fibrinogen release from a stressed liver, and even a hit on bone marrow, to prevent the release of FAT, STICKY PLATELETS!!!!!
A similar Medit. diet, in the PREDIMED study in Barcelona, prevented heart and stroke by 30% in cases selected for CVD risk, but without an actual history of such previously. Of note, Medit Diet plus 30g/day of mixed NUTS [more inositol!!!} gave 50% protection against stroke.
And we all remember Dr Dean Ornish’s small but useful Diet Heart Study, from the mid-1990s, with striking and rapid improvements seen with a plant-based, grainy-beamy-nutty diet. See his heart-felt essay STATINS AND THE SOUL OF MEDICINE. He claims his diet got cholesterol down as well as any statin.
I am writing to Dr Ramon Estruch in Barcelona, proposing we do a small follow-up study, called PREDIMED PLUS, in which we IDENTIFY the WORRIERS [as Sir William Osler called heart attack victims in 1905!!], and RAMP UP the inositol intake, by adding 5 gm/day of cheap Minnesota Corn Belt inositol, at 35 cents/day for 5 GM!!! That dose, added to the 1.5 gm already in the wholegrain, legumes, nut and citrus, should WIPE OUT A=HAD-IT–COMPLETELY.
ADIOS, STATINS–except for post-AMI cases, who should get everything we can throw at them, including any statin benefits that MAY not be available from supplementary inositol. But note: the plant-based Medit diet is YUMMY, and so is my sweet-tasting inositol powder supplement. Anxious cases LOVE IT–they actually NOTICE the benefit within days–unusual calmness and confidence, better sleep [with sweet dreams, and FRESH on waking], outstanding stamina within a week [partly due to anti-ageing mitochondrial biogenesis], better libido, faster growth of nails and hair, and a distinct lift in COGNITION.
In such a good mood, our heart attack patient may be more inclined to stick with their statins as well–but, ironically, they may no longer need them. I would suggest a compromise–push the Medit diet and the 5 gm/day inositol, AND the statins, but drop the latter after 6 months or so. And don’t forget to remind them all about the deluxe anti-ageing genes–over 500 induced, with huge hits on life-extending immune defence, on physical energy, and on QUICK THINKING [already proven with wholegrain cereal, in Welsh primary school kids–a late-morning cognitive lift was seen throughout the class].
So with inositol patients can enjoy the wonders of both Medicine AND Science!!!
The statin hysteria on the internet is to blame. If the general public will not listen to doctors then who is to blame??
What exactly is the absolute risk reduction of a recurrence of ACS in patients put on highest dose vs a dose that controls the Lipids with guidelines?
What is the actual REAL impact of ststins in these patients?
Where are the long term studies? for this opinion.