Heart Attack Risk
Drug may one day save my life
His father died of a heart attack, so Dr Lawrence Seymour decided to try to protect himself from the same fate
Shortly before I qualified as a doctor, I drew up a personal 10-year health plan. In it, I speculated that, come my 35th birthday, I would opt for taking statins - cholesterol- lowering drugs - as a preventative measure against coronary artery disease.
Heart attack prevention
Prevention: statins are a safeguard against the all-important first heart attack
Let me explain. My father, a Master in the Merchant Navy, succumbed to the cardiac “widow maker” - a massive heart attack that strikes without warning in middle age. He was 52 and died bringing his ship alongside in Galveston, Texas. A crewman on the bridge described how he crashed to the deck, smashing his glasses. He never regained consciousness, despite cardiac massage by fellow officers.
It was 1982, and none of the early intervention procedures that are now routine were in place. Today, defibrillators are increasingly available in public places; some paramedics liaise with emergency departments to administer clot-busting agents at the scene; and medics aim to do the same within seven minutes of a victim’s arrival at hospital - the “door to needle time”, in ER-speak.
Furthermore, we now have access to statins, a safeguard against the all-important first heart attack (myocardial infarction) and in arresting progression of heart disease. Public awareness of the drugs is high: they have been available in the UK without prescription since 2004. It is estimated that up to three million Britons take them, and government plans announced last week for health checks for every person aged 40 to 74 could see that number double, with dramatic impact on the NHS drugs budget. Critics say the drugs have limited effectiveness. Well, I, for one, will take the chance.
From the 1970s, coronary artery disease cut a swathe through a generation of overweight middle-aged men. In my early teens, I remember finding my father’s post-mortem report in a wardrobe. It was brutally concise: there was “diffuse atheroma” (fatty streaks) throughout the blood vessels of his heart.
Angina (chest pain on exertion) and myocardial infarction were rare before 1900, yet within 80 years heart disease was causing a third of all deaths in the West.
In the postwar/post-ration era, millions of men unwittingly smoked and ate their way to an early grave, unwilling participants in an evolutionary cull - where being predisposed to high blood pressure (hypertension) and an inability to deal with fatty/salty foods resulted in premature death. In Darwinian terms, they were not fit, they didn’t survive and the consequences were tragic for families like mine.
My family history suggested a predisposition to early hypertension - my paternal grandfather had died at 48 from the consequences of uncontrolled hypertension. So from early adulthood, I was a self-perceived “cardiac event” waiting to happen.
At medical school, off-the-cuff comments by lecturers seemed to be made for my benefit alone, and were scribbled down and memorised. One cardiologist explained that most of us would develop atheroma in our arteries. In his opinion, the lesions were of two types. The first comprised fibrous, calcified strips, which he compared to “polo mint-like” narrowings within the vessel walls. They were typically seen in older people who knew that, on walking 50 yards, they would experience angina due to the reduced blood supply to the heart. Even though these lesions often blocked up to 90 per cent of the vessel, the angina sufferer could go on for years with the odd spray of nitrate puffer under the tongue to get them up the next incline.
The second type of lesion my tutor compared to cholesterol-filled “scabs”, which caused relatively minor narrowings but were prone to rupture and bleeding. A clot forming on the “scab” could rapidly block the vessel, bringing the heart to a standstill as the victim fell to the floor. “What you want, fellas, is polo mints, not scabs,” he told us.
The case of Sir Ranulph Fiennes, the Polar explorer, is a perfect illustration of what he meant - and of remarkable advances in the way emergency services have adapted to the pandemic of coronary heart disease. In June 2003, Sir Ranulph had just boarded a plane when one of his coronary “scabs” ruptured, causing arrest. Luckily for him, a nearby fire crew, with the equipment and training, were at hand to apply a shock across his chest and restore life. His heart stopped a further five times in the next two hours before he received cardiac bypass surgery.
The patient in this case was an endurance athlete, for whom an average day would be a marathon in the Scottish Highlands. He had been able to perform vigorous exercise, without symptoms, yet his arteries became dangerously diseased. Happily, Sir Ranulph recovered, and once his vessels were replumbed, went on to do seven marathons on seven continents in seven days.
My mid-30s MOT showed my cholesterol profile to be reasonable, with a total count of less than five, as recommended by NICE (National Institute for Clinical Excellence). My “bad” LDL cholesterol was 2.7 (the goal is less than three) and my “good” HDL cholesterol was 1.4 (more than one is a healthy reading for men; above 1.3 is right for women). However, a chat with a colleague in the lipid clinic swayed me towards my original plan of statins as a proactive measure. “With your family history,” he said, ”why would you not?”
The millions of prescriptions written worldwide confirm that statins are safe to take. The most significant side-effect is a reversible inflammation of muscle tissues, seen in less than 0.01 per cent of recipients. As with any drug, extreme side effects are occasionally reported: in the case of statins, these are fatalities due to renal failure, with an incident of 0.15 cases per million prescriptions. Similarly, abnormalities reported in liver function are rarely significant and almost always reversible on cessation of the tablet. This favourable risk-benefit analysis of the disease that kills more middle-aged men than all other diseases together has led some to compare statins with antibiotics in their ability to reduce the burden of disease worldwide.
No doubt, there will be some reading this who will be suspicious of this medic’s enthusiasm for statins. Well, on a shelf in my office is a coffee mug bearing the name of a particular brand. That is the only support I have received from a statins manufacturer and, for the record, I am not on the payroll of any pharmaceutical organisation.
The benefits of statins in high-risk groups are indisputable; it’s the use of cholesterol-lowering agents in patients without clear-cut risk factors that is controversial. Most doctors, myself included, would be unwilling to expose patients to side effects when the presence of disease is uncertain. But we commonly see heart disease in people with normal cholesterol, and evidence suggests this group still benefit from statins following a heart attack.
After 10 years working with the hospital crash team, I decided to reverse the risk factors I could control. I have increased my intake of fresh fruit, vegetables, oily fish and red wine, and I’m training for a half-marathon.
In addition, despite a normal cholesterol profile, I have opted for statins in the belief that for me - and I stress this is a personal decision - the benefits outweigh the risks. In the words of my old teacher, what I’m aiming for are “polo mints, not scabs”. I hope my two brothers are reading this.
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