When blood vessels go wrong, why are we better at treating the heart than the head?

The strange discrepancies between how we treat strokes and heart attacks.

When I started practice in the early 1990s, medical attitudes to strokes and heart attacks couldn’t have contrasted more starkly.

Heart attacks were often dramatic and challenging; there were plenty of treatments to deploy, and much high-tech gadgetry to play with. Good outcomes were immensely satisfying, a confirmation that medicine made a difference. A stroke, on the other hand, felt like a depressing fait accompli. There was little to be done by way of treatment, survival was a matter of chance, and many patients were left with profound disabilities from which any recovery was painstaking and marginal.

The pathology underlying the two conditions is broadly similar. Every organ relies on uninterrupted perfusion of blood for its oxygen and nutrition. Clearly blood has to be liquid in order to circulate, yet it is also chock-full of tiny platelet cells, and a soluble chemical, fibrinogen, that will solidify into a clot at a moment’s notice. Blood vessels are lined with the biological equivalent of Teflon – the vascular endothelium – which ensures this clotting potential is held in check. Any breach in this endothelium activates the platelets, causing them to clump together in great numbers and to convert fibrinogen into its insoluble cousin, fibrin, which coagulates into a matted web.

This clotting cascade is vital in trauma, sealing damaged vessels and limiting blood loss; but when it is triggered in other circumstances, it can have catastrophic effects.

Cholesterol-rich plaques in arterial walls – the “furring up” of popular discourse – can swell and rupture the vascular endothelium. The ensuing clot may block the vessel entirely, causing death to the tissues downstream. If this occurs in a coronary artery, heart muscle dies – a myocardial infarction (MI), or heart attack. In the brain, the result is a stroke.

In the UK, deaths due to MI halved between 2002 and 2010. Some of this dramatic drop is because heart disease is becoming less common, thanks to the decline in smoking, and improvements in diet and exercise. The NHS has also become better at identifying and offering preventative medication to those at high risk. But around 50 per cent of the astounding increase in survival comes down to the transformation in treatment of those who have the misfortune to suffer a heart attack.

The management of MI has been revolutionised by techniques to unblock occluded coronary vessels, thereby salvaging as much of the blood-starved heart muscle as possible. The earliest attempts used “clot-buster” drugs known as thrombolytics, which cause the fibrin in the offending clot to dissolve. Thrombolytics still have an important place, but surgical approaches are ever more commonplace.

Angioplasty, where a wire is threaded up to the coronary vessels from an artery in the groin, has become the first-line emergency treatment for the most serious types of MI. A balloon at the end of the wire, or an implantable wire cage called a stent, can be deployed to reopen the blocked vessel.

Time is of the essence: the earlier that perfusion can be restored, the less heart muscle will die, and the better the outcome (in some cases, MI can actually be aborted). Ambulance services, and A&E and cardiology departments, have refined protocols for fast-tracking suspected MI sufferers, and “door-to-needle” or “door-to-balloon” times have been reduced substantially.

Stroke medicine has also undergone a revolution in recent years. Thanks to a sustained research effort led by the Stroke Association, much more is understood about maximising recovery following stroke, and most sufferers will now be treated in a dedicated stroke unit, which significantly improves outcomes.

The holy grail, though, would be comparable success in re-perfusing blood-starved tissue after stroke to what cardiologists are achieving in MI.

Stroke is different in a number of ways. Angioplasty is not useful in the majority due to the small size of the vessels within the brain. Thrombolysis should, in theory, be successful – but whereas re-perfusion can salvage heart muscle up to 12 hours after the onset of symptoms, brain tissue has a much narrower window of opportunity, probably around three to four hours.

And not all strokes are caused by clot. Around one in ten occur when a blood vessel ruptures and bleeds into the surrounding brain; you most certainly don’t want to give clot-busting drugs in those cases. They can be identified on a scan, but more challenging to predict are those patients suffering a clot-induced stroke who go on to bleed into the damaged neural tissue, something thrombolytics also make catastrophically worse.

The balance between benefit and harm is a fine one, and some experts have recently called for thrombolysis in stroke to be confined to clinical trials until the evidence to justify its use is clarified.

For now, at least, we continue to rescue the heart more successfully than the head.

Phil Whitaker is an award-winning novelist and a working doctor

Doctors treat a heart attack patient in Berlin, Germany. Image: Getty

This article first appeared in the 30 October 2013 issue of the New Statesman, Should you bother to vote?

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The section on climate change has already disappeared from the White House website

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The perfect summary of Trump's attitude to global warming.

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