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Coronary Disease| Muscle Pain|Heart Rate

Posted Nov 09 2008 10:09pm

Sunday, November 09, 2008

There is increasing evidence that increased heartrate may be an independent risk factor for cardiovascular morbidity and mortality both in patients with ischaemic heart disease and in the general population. Elevated heartrate in coronary artery disease is a major determinant of oxygen consumption and appears to evoke most episodes of ischaemia. Increased resting heartrate may also contribute to the development of atherosclerosis, facilitate plaque destabilisation and initiate arrhythmias, leading to acute coronary events and sudden death. Reducing heartrate is a central aim in the treatment of stable angina pectoris; this therapeutic approach may have an essential role in lowering the incidence of cardiovascular morbidity and mortality in patients with pre-existing ischaemic heart disease. However, this heartrate hypothesis has not thus far been proven. Evidence suggests that the use of heartrate -lowering drugs may have a beneficial effect; however, most treatments for angina have additional negative inotropic effects on the heart. This hypothesis can now be tested following the recent development of selective heartrate drugs. 

There is increasing evidence that increased heartrate may be an independent risk factor for cardiovascular morbidity and mortality both in patients with ischaemic heart disease and in the general population. Elevated heartrate in coronary artery disease is a major determinant of oxygen consumption and appears to evoke most episodes of ischaemia. Increased resting heartrate may also contribute to the development of atherosclerosis, facilitate plaque destabilisation and initiate arrhythmias, leading to acute coronary events and sudden death. Reducing heartrate is a central aim in the treatment of stable angina pectoris; this therapeutic approach may have an essential role in lowering the incidence of cardiovascular morbidity and mortality in patients with pre-existing ischaemic heart disease. However, this heartrate hypothesis has not thus far been proven. Evidence suggests that the use of heartrate -lowering drugs may have a beneficial effect; however, most treatments for angina have additional negative inotropic effects on the heart. This hypothesis can now be tested following the recent development of selective heartrate drugs. 

Increased heart rate may be considered as a true risk factor for atherosclerosis. Increased heart rate favours the occurrence of injury to the arterial wall, which may perturb intracellular junctions, increase permeability of the endothelial cells, and favour atherogenesis.   Resting heart rate is an indicator of risk for cardiovascular mortality.   Patients with chronic heart failure or following acute myocardial infarction, a reduction of 1 beat/min was associated with a 2% reduction in death.   Overall, cumulative data from several studies suggest that resting heart rate greater than 80 beats/min significantly increases risk of cardiovascular morbidity and mortality. Patients with a heart rate of at least 80 beats/min were almost twice as likely to suffer cardiovascular mortality as those with a lower heart rate.(Hall AS. Palmer S. Theheartratehypothesis: ready to be tested.   Heart. 94(5):561-5, 2008)

Patients with nerve related muscle pain tend to have higher heart rates.  eToims have been shown to lower heart rate in such patients from a combined ability to lower the sympathetic discharge as well as from effects of vagal stimulation without pharmaceutical means. (Chu J, Schwartz  I: eToims Twitch Relief Method in Chronic Refractory Myofascial Pain (CRMP). Electromyogr Clin Neurophysiol 48: 311-320, 2008)

 

www.stopmusclepain.com

 

eToims, muscle pain

 

coronary disease, eToims, Heart rate, muscle pain, pain
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