Around a decade ago, there was significant publicity around the Economy syndrome. A handful of people travelling on long haul flights when they arrived at their destination (or soon after) developed painful, swollen legs and were found to have clots related to many hours of sitting cramped in the economy section of the plane.

These people wanted to sue Qantas but, in reality, should be suing their parents for giving them the genes that led to excessive blood thickening. Around 1% of the population carry one of the variety of genes that predispose to clotting, typically during periods of immobilisation. The immobilisation is the precipitant but not the cause.

The same can be said for the occasional young woman who takes the pill and within a month has suffered a stroke. Hormone therapies can increase blood thickness but typically this is only clinically relevant in people with a genetic predisposition to clotting. Therefore, again, instead of suing the pharmaceutical company that makes the contraceptive pill, the affected person should be suing their relatives for exactly the same reason I have given above.

These genetic abnormalities range from the most common Factor V Leiden to the rather uncommon Anti-thrombin 3 deficiency. If you have a strong family history of any form of clotting, such as deep venous thromboses, pulmonary emboli (clots travelling into the lungs) that affect the venous side of the circulation, or even a very strong family history of arterial clotting, such as recurrent heart attacks or stroke, then there could be a familial predisposition to clotting. There are specific blood tests that can be performed to determine these conditions.

Blood thinners have been available for a number of years, mainly in the form of warfarin or the much weaker aspirin. Aspirin is inappropriate for venous clotting or clots in the lower pressure chambers in the heart i.e. the atriae but typically covers most forms of arterial clotting, although over the past 10 years the evidence has grown to support often using two forms of antiplatelet agents that include aspirin.

Over the past decade, new stronger anticoagulant agents have replaced warfarin in many cases, apart from long-term use with mechanical heart valves.

Research by the superb Baker Heart and Diabetes Institute in Melbourne, in conjunction with Harvard University recently published in the Journal of Clinical Investigation Insight, has discovered a new antibody that purely targets fresh clots. This only works on activated platelets, which are the sticky cells that form part of a clot along with the protein clotting factors but leaves normal components of clotting alone and thus markedly reduces any risk of bleeding that can occur with all of our existing clotting agents, including aspirin up to the newer stronger oral anticoagulants.

Thus, people with a strong predisposition to clotting or a prior history of thromboses could have an injection of this antibody prior to travel, or an operation as pure prevention. This may also have a place in the management of heart attack and stroke, dissolving fresh clots that occur in this situation.

To date, the antibody has proven enormously successful in laboratory animals and human blood but it needs to be trialled for clinical safety in humans. It will probably not be available for clinical use for at least five to 10 years but, if proven safe in humans, which is highly likely, this will be a major breakthrough in the prevention and treatment of blood clotting.