“I am going to die in the saddle.”
On one of his luckier days, Howard Hughes, the free-wheeling film mogul, chanced upon one Jane Russell, a feisty and strong-willed 19-year-old starlet from Bemidji, Minnesota. Being able to do whatever he wished in his own studio, Hughes cast Russell in his latest film, “The Outlaw”, as the lascivious Rio, a role which propelled her into instant and precocious celebrity.
Finely tweaked by Hughes, her amply displayed bosom was immediately censored as illegally indecent under America’s puritanical Hay’s Code. This was 1943, the bloody apogee of the Second World War, and Jane Russell had become the fanciest pin up of all time (except Betty Grable, of course).
As Bob Hope wryly put it, “Culture is the ability to describe Jane Russell without moving your hands”.
Being a force of nature with a rugged Scottish ancestry, Russell had determined to die in the saddle, to die on the job – which she did, aged 89. Battling through alcoholism, infertility, relationships, adoptions, becoming a born-again Christian, to establish WAIF to find homes for 40,000 orphans, she was known to all for her generosity, good humour and congeniality.
I am pretty sure that Jane Russell had not quite cottoned on that “to die in the saddle” was a European double entendre. The French know it as la mort d’amour, fondly associated by older men with illicit sex – which could have some truth.
In 2019, a Paris court found a company liable for the death of an employee who had a cardiac arrest shortly after having had sex with “a stranger” on a business trip: on appeal, the decision was upheld, as sexual activity was normal, “like taking a shower or a meal”, and “an employee on a business trip is entitled to social protection over the whole time of his mission, and regardless of the circumstances”.
Just how common is dying in the saddle, one asks.
In 2017, a study of 38,000 medicolegal autopsies over a period of 45 years demonstrated that there had been 99 cases of natural death associated with sexual activity (0.26%). Most deaths occurred, at median age 57 years, during extramarital sex in males who had pre-existing heart disease and/or were overweight or obese (1).
Well, that is relatively reassuring to middle-aged men, as long as you are slim, and your heart is in good shape. You can do something about your weight, cholesterol, and blood pressure, but how do you know about the state of your coronary arteries?
For many years you have been carefully tutored to believe that a high cholesterol is responsible for the formation of dangerous fatty deposits, “plaque”, in your arteries. As of now, this is not at all true; cholesterol plaque is driven by your genes. Thus, you can have a high cholesterol without plaque formation, and, conversely, a reasonable cholesterol level with prolific plaque deposits. It is the genes that matter most, not the cholesterol. (2)
Exactly which particular genes are responsible for plaque formation have yet to be identified, but their presence is ascertained through an estimate calculated by comparing an individual’s genotype profile with relevant data from the Genome-wide Association Study (GWAS). The result is a “polygenic risk score” (Nature Protocols, 24 July 2020).
The extent to which coronary arteries are affected by plaque, the “plaque burden”, is imaged by computed tomography (CT) scanner. Individual plaque formations are identified through the presence of calcium in the more mature deposits, and the total calcium volume in the coronary artery tree, the “coronary artery calcium score” (CACS), is used to compute the risk of obstruction to the blood flow to the myocardium, the heart muscle.
A zero CACS implies that you have no mature plaque and little or no propensity to develop dangerous cholesterol plaque in the future, i.e., you will have a low polygenic risk score (PRS). On the other hand, confusingly, a high CACS does not necessarily indicate an immediate threat, as plaque can be spread widely and thinly throughout the coronary artery tree without causing much significant narrowing.
In an ideal world, angiography, virtual or radiological, solves this problem by visualising the internal configuration of the coronary arteries, identifying any plaque which threatens to occlude blood supply, and enabling this to be squashed (by balloon angioplasty) and held back by tiny tubes (stents), or, if totally impracticable, by coronary artery bypass grafting.
Unfortunately, the NHS has financing problems which preclude a flexible approach to coronary artery disease. The false assumption has been established that all patients with a high cholesterol are at high risk of developing coronary artery disease. Hopefully, the introduction of an automated and low-cost PRS protocol will dislodge the makeshift option of life-long statin therapy for each and every case. There must be some anxiety in government that any reform or relaxation of the present rigid, formulaic process of treating the most common cause of death in the UK could create political repercussions: about 18.2 million adults have coronary heart disease, around 370,000 a year die from it.
It is my view that we, the public, should take considerably more notice of our cardiac health. We should be extremely alarmed by our vulnerability to COVID with its proclivity to strike down young and old suffering from cardiovascular disease and its cohorts of obesity, high blood pressure and diabetes. To expect government to dictate our lifestyle and diet should seem bizarre, but, as 65% of our population are fat or obese, do government have an option? I think not.