New research casts doubt over heart disease treatments

High blood pressure is sometimes treated by calcium channel blockers to reduce the heart beat, as the channels – which allow calcium into the cells – are linked to muscle contraction. But the channels are also fundamental to the electrical currents which create the heartbeat.

University of Leeds scientists Dr Matthew Lancaster and Dr Sandra Jones have discovered that the channels gradually fail as we age and this failure is a likely factor in arrythmia and heart attacks in the elderly. By blocking the channels to treat high blood pressure, clinicians may unwittingly be increasing the likelihood of other problems developing.

Dr Lancaster said: “Many people suffer from an irregular heartbeat as they grow older and large numbers have pacemakers fitted. Making the link between these heart problems and the failure of the calcium channels as we age has flagged up a warning sign that some common medical treatments may be making the condition worse. Clinicians should think carefully before prescribing calcium channel blockers and ensure that, in treating one heart condition, they aren’t exacerbating others.”

The beating of the heart is caused by an electrical signal, which starts at the top of the heart in the sinoatrial (SA) node and is transmitted down to cause consecutive muscle contraction of the different chambers. The electrical signal is generated through an influx of calcium into the cells in the SA node, causing a change in voltage which creates the current.

Calcium enters the cells through channels – so these are fundamental to a steady heart beat. If the calcium channels are reduced, the heartbeat becomes irregular leading to a fall in blood pressure, fainting, and potentially, if untreated, death. These are the symptoms which can mean a patient needs a cardiac pacemaker fitted – but they may be exacerbated by treatment for high blood pressure which blocks the calcium channels.

The link between age and loss of calcium channels opens up new possibilities of treating heart conditions. Dr Jones said: “It may be possible to mitigate the effects of the loss of calcium channels through gene therapy, as the treatment would only be required in one specific area – the sinoatrial node – so should be fairly easy to administer.”

The researchers also think exercise may also be a factor. As members of the sports science group in Leeds’ Faculty of Biological Sciences, Drs Lancaster and Jones are now looking at whether exercise training is able to reduce the loss of the calcium channels in the SA node.

The research is published this week in the journal of the American Heart Association, Circulation.