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Rapid Responses: Rapid Responses published:
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Higher resting pulse rates with coronary disease, strokes and migraine
- Ellen C Grant (5 February 2009)
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Pulse Mass Index and cardiac risk in women
- Enrique J. Sánchez-Delgado (5 February 2009)
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Women, heart rate and coronary disease. Cause or consequence?
- Carlos Escobar, Rocio Echarri, Vivencio Barrios (9 February 2009)
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Thyroid dysfunction deserves attention
- Takeharu Koga, Tomoko Kamimura, Munetsugu Nishimura (11 February 2009)
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Resting Heart Rate as a Low Tech Predictor of Coronary Events in Women – Comment
- Gila Perk, Michael Bursztyn (11 February 2009)
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Resting heart rate, blood viscosity and ejection fraction.
- Leslie O Simpson (11 March 2009)
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Not every stress is evil - about heart rate and shear stress
- Pascal Meier, Steffen Gloekler, Tobias Traupe, Stefano de Marchi , Christian Seiler (13 March 2009)
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What about absolute risks?
- Michael J Campbell, University of Sheffield S1 4DA (13 March 2009)
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Heartbeat Bank
- Peter AF Watson (14 March 2009)
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Coronary Heart Disease and Autonomic Nervous System
- John Arthur Lee (17 March 2009)
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Tachycardia: cause or effect?
- Richard G Fiddian-Green (18 March 2009)
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So what about heart rate variability.....?
- William E Moody (19 March 2009)
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Re: heart rate variability.
- Richard G Fiddian-Green (20 March 2009)
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Ellen C Grant, physician and medical gynaecologist Kingston-upon-Thames, KT2 7JU
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It is interesting but not unexpected that Women’s Health Initiative Research Group finds more risk of coronary events in women with higher resting pulse rates.1 The authors conclude that there was no similar increased risk of stroke. However, in Table 2, women with resting pulse rates above 70 beats per minutes had increased hazard ratios for stroke at 1.21 (1.06-1.38) and 1.23 (1.07-1.41) which are significant. The relationship with resting pulse rate and vascular disease is easily demonstrated in patients with headache or migraine. A pulse test helps to reveal responses to individual foods. In my paper, Food allergies and migraine, Lancet 1979, Figure 2 shows the changes in pulse rate and appearance of symptoms in a migraine patient during food testing. Patients, who still had headaches after stopping smoking or using hormones or other medications, followed a 5 day low-allergy diet of lamb and pears as recommended by Dr John Mansfield. Individual foods then were re- introduced at each meal. Resting pulse rates increased over the next 90 minutes after eating a food causing symptoms such as headaches or indigestion. When such foods were excluded, 60 patients followed a low allergy diet. All 60 patients improved and 51 (85%) become headache-free. 15 of these migraine patients also had hypertension. All became normotensive eating a low-allergy diet. Daily medications were no longer needed. I have continued to advocate high protein/low allergy diets for my preconception patients since then. The commonest foods causing pulse changes are wheat, corn and cane sugar, coffee, tea, yeast, oranges and eggs. It is clearly often possible to lower resting pulse rates with simple means. 1 Hsia H, Larson JC, Ockene JK, et al, and for the Women’s Health Initiative Research Group. Resting heart rate as a low tech predictor of coronary events in women: prospective cohort study. BMJ 2009;338:b219. 2 Grant ECG. Food Allergies and Migraine. Lancet 1979:1:966-968. Competing interests: None declared |
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Enrique J. Sánchez-Delgado, Internal Medicine-Clinical Pharmacology. Director of Medical Education Hospital Metropolitano Vivan Pellas, Managua, Nicaragua
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Pulse Mass Index and cardiac risk in women The study WHI has given us, since their first publication, important information on the cardiac risk of postmenopausal women. Now, Judith Hsia et. al. (BMJ 3 February 2009), confirm, in 129 135 postmenopausal women followed for 7.8 years, that an elevated resting heart rate (RHR), a low tech and inexpensive measure of autonomic tone, independently predicts myocardial infarction or coronary death in women, and show that the coronary risk was 26% higher among women with RHR over 76 bpm versus 62 bpm or less. They found this risk large enough to be clinically meaningful. Their findings are in general agreement with other recent studies, like BEAUTIFUL and EUROPA (ESC, Munich, Sept. 2008), the QRISK 2 (BMJ 28 June 2008), in which Julia Hippisley-Cox et. al. use 14 risk factors to predict the cardiovascular risk, including Body Mass Index (BMI), and others, that can have an influence in the resting heart rate, like smoking, deprivation, atrial fibrillation, type 2 diabetes and rheumatoid arthritis, and the report from Aage Tverdal et. al. on heart rate and mortality from cardiovascular causes (EHJ November 2, 2008), who shows that a high RHR (or other risk factors that increase the RHR) is associated with an unfavourable pattern of risk factors and may be a marker for sympathetic nervous system activity. All the major CV risk factors – cholesterol, triglycerides, blood pressure, body mass index, family history of CV disease, smoking, and sedentary lifestyle – increased significantly across increasing quartiles of RHR. In the recent years, also, the BMI has been accepted as a main cardiac risk factor (not any more a second range risk), as reported by Wilson PW, et al. (Circulation July 8 2008) who found that 1-SD unit (4.33 kg/m2) of BMI imparted a 28% effect on risk of initial CVD events. It was estimated that 67% of the BMI effects appear to operate through the ratio of cholesterol to high-density lipoprotein cholesterol, systolic blood pressure, and diabetes mellitus. Recently the British Medical Journal (5 August 2008) comments that Body mass index can be added to the list of traditional cardiovascular risk factors (high systolic blood pressure, higher ratio of cholesterol to high density lipoprotein cholesterol, and diabetes) for predicting first coronary heart disease events. Ten year ago, we published our findings on the Pulse Mass Index in The Lancet (March 13, 1999) and more recently, actualized, in the World Congress of Internal Medicine, in Buenos Aires, Argentina, September 19, 2008. The mentioned studies, including now the WHI, are in agreement with our findings validated during this decade long, in over 1650 men and women over 40 years old. The Pulse Mass Index (Resting Heart Rate multiplied by the Body Mass Index and divided by 1730), has a very high (95%) correlation with the Framingham Risk Score. A Pulse Mass Index over 1.3 indicates with a high probability a high cardiovascular risk and the possible need of a more complete evaluation (eg. exercise EKG or Coronary CT or calcium score) and management of the CV risk factors in these patients. Since our first report we explained that we correlated the Pulse or RHR with the BMI, because the RHR reflects the oxidative metabolic rate and activity of the sympathetic nervous system, such as under stress, obesity or hyperinsulinemia and that these findings probably indicate the relation between hyperinsulinemia, stimulation of the sympathetic nervous system, and oxidative metabolism that is seen in obese patients and which improves when they exercise regularly or lose weight. The Pulse Mass Index is also the most simple and economical first clinical approach to the risk evaluation in a large population of both men and women, and more so in the developing countries, where around 80% of all cardiovascular deaths occur. Prof. Enrique Sánchez Delgado, MD
Competing interests: None declared |
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Carlos Escobar, Cardiologist Hospital Infanta Sofia, Paseo de Europa 34, 28702, SanSebastian de los Reyes, Madrid, Spain, Rocio Echarri, Vivencio Barrios
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We read with interest the manuscript of Hsia et al focused on the impact of resting heart rate as a predictor of coronary events in women (1). For this purpose, authors performed a prospective cohort study from The Women`s Health Initiative database, that was undertaken at 40 research clinics in the United States. Overall, a total of 129,135 postmenopausal women were included. After a 8 years follow-up, higher resting heart rate was independently associated with coronary events, but not with stroke. Several studies have suggested that higher heart rate is a cardiovascular risk factor and taking into account that the best approach in the treatment and prevention of coronary heart disease is the aggressive control of all risk factors and comorbidities, it is likely that heart rate could be included in the next guidelines (2). Cardiovascular disease is the most important cause of death among women. Despite that, it seems that many physicians and patients do not actually perceive the coronary risk in women and this could be related with the well-known cardioprotective effect of feminine hormones but also to the lack of information about cardiovascular prognosis in women in the past decades (3). Fortunately, there is a growing interest about the importance of cardiovascular prevention and treatment of women. Epidemiological studies have reported that when compared the same population of patients with chronic ischemic heart disease, women have more risk factors and comorbidities than men, including higher heart rate, and with worse blood pressure and LDL-cholesterol control rates (3,4). In this context, is heart rate a risk factor or a marker of risk in women? In other words, is heart rate the cause or the consequence of the worse cardiovascular prognosis? Probably both. It could be the cause because higher heart rate increases by itself coronary events; but since it reflects an underuse of some drugs that have been proved to be useful in this population such as beta blockers it could be also a consequence. In conclusion, since, as authors reported, resting heart rate is an easy and inexpensive measure of autonomic tone, independently predicts myocardial infarction or coronary death, physicians should pay more attention to it in general population, but particularly in postmenopausal women. 1. Hsia J, Larson JC, Ockene JK, Sarto GE, Allison MA, Hendrix SL, et al. Resting heart rate as a low tech predictor of coronary events in women: prospective cohort study. BMJ 2009;338:b219, doi: 10.1136/bmj.b219. 2. Fox K, Borer JS, Camm AJ, Danchin N, Ferrari R, Lopez Sendon JL, et al. Resting heart rate in cardiovascular disease. J Am Coll Cardiol. 2007;50:823-30. 3. Barrios V, Escobar C, Bertomeu V, Murga N, de Pablo C, Calderon A. Sex differences in the hypertensive population with chronic ischemic heart disease. J Clin Hypertens (Greenwich). 2008;10:779-86. 4. Barrios V, Escobar C, Bertomeu V, Murga N, de Pablo C, Asin E. High heart rate: More than a risk factor. Lessons from a clinical practice survey. Int J Cardiol. 2008 Aug 4. [Epub ahead of print] Competing interests: None declared |
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Takeharu Koga, Vice-director Asakura Medical Association Hospital, Tomoko Kamimura, Munetsugu Nishimura
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When it comes to the underlying mechanism for the finding that an increased resting heart rate is associated with an increased incidence of coronary heart disease (CHD) in women, thyroid dysfunction, a relatively common disorder in women, deserves attention as a possible explanation. As was illustrated in meta-analyses 1 2, numerous studies have noted that thyroid dysfunction, even in subclinical form, is associated with an increased risk of CHD. Although an increase in heart rate is well-recognized in hyperthyroidism, hypothyroidism is associated with impaired heart rate control 3, cardiac 4 and coronary functions 5, which may result in an increased resting heart rate. Interestingly, thyroid dysfunction was associated with an increased incidence of CHD but not with that of cerebrovascular disease 6 in concert with the finding by the authors. Counting resting heart rate seems to be not merely a useful clinical tool predicting cardiovascular incidence but also open window for further research leading to better understanding and management. 1. Ochs N, Auer R, Bauer DC, Nanchen D, Gussekloo J, Cornuz J, et al. Meta- analysis: subclinical thyroid dysfunction and the risk for coronary heart disease and mortality. Ann Intern Med 2008;148(11):832-45. 2. Rodondi N, Aujesky D, Vittinghoff E, Cornuz J, Bauer DC. Subclinical hypothyroidism and the risk of coronary heart disease: a meta-analysis. Am J Med 2006;119(7):541-51. 3. Galetta F, Franzoni F, Fallahi P, Tocchini L, Braccini L, Santoro G, et al. Changes in heart rate variability and QT dispersion in patients with overt hypothyroidism. Eur J Endocrinol 2008;158(1):85-90. 4. Biondi B, Palmieri EA, Lombardi G, Fazio S. Effects of subclinical thyroid dysfunction on the heart. Ann Intern Med 2002;137(11):904-14. 5. Baycan S, Erdogan D, Caliskan M, Pamuk BO, Ciftci O, Gullu H, et al. Coronary flow reserve is impaired in subclinical hypothyroidism. Clin Cardiol 2007;30(11):562-6. 6. Flynn RW, Macdonald TM, Jung RT, Morris AD, Leese GP. Mortality and vascular outcomes in patients treated for thyroid dysfunction. J Clin Endocrinol Metab 2006;91(6):2159-64. Competing interests: None declared |
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Gila Perk, Faculty, Department of Cardiology 10016, Michael Bursztyn
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We read with interest the recently published article Resting Heart Rate as Low Tech Predictor of Coronary Events in Women: Prospective Cohort Study, by Hsia and colleagues, regarding the predictive value of resting heart rate in women.. The association between higher heart rate and increased prevalence of coronary events was stronger for the younger cohort than the older cohort. We previously studied the relationship between resting heart rate and mortality in an elderly population from the Jerusalem 70-year-old cohort. We have shown that in this population, resting heart rate (as measured both by pulse counting as well by electrocardiograms) was an independent predictor of mortality among women aged 70 years, who were followed for 6 years (ROR for death 3.71, 95% CI 1.41-9.8). This association was independent of previous cardiovascular or cerebrocascular disease, congestive heart failure, anemia, and other risk factors including hypertension, smoking, and level of exercise or activities of daily living. When women treated with beta blockers were excluded, this relationship became even stronger (ROR for death 8.86, 95% CI 2.17-36.23). We found a very good correlation between palpated pulse rate and electrocardiographic hear rate (correlation coefficient 0.79, p=0.0001). The relationships between heart rate and mortality were similar whether the palpated pulse or the electrocardiographic one were employed. Of note, in our data we controlled for the presence of anemia, which may be more prevalent among the elderly, and may have been a confounder in Hsia’s study. Prior studies have also demonstrated that increasing heart rate may be related to increased cardiovascular mortality in different age groups, both in men and in women (3,4). With these in mind, our data, and the current paper by Hsia and colleagues, we join the authors in their conclusion that heart rate may be an independent, “low tech” low cost indicator of general health. In this age of increasing costs for sophisticated risk-stratification tools, it seems that such a simple measure of general health status should be welcomed, and efforts should be directed at understanding how to use this information for improved health outcomes. References: 1.Hsia J, Larson JC, Ockene JK, Sarto GE, Allison MA, Hendrix SL, Robinson JG, LaCroix AZ, Manson JE; Women's Health Initiative Research Group. Resting heart rate as a low tech predictor of coronary events in women: prospective cohort study. BMJ. 2009 Feb 3;338:b219. 2.Perk G, Stessman J, Ginsberg G, Bursztyn M. Sex differences in the effect of heart rate on mortality in the elderly. J Am Geriatr Soc. 2003 Sep;51(9):1260-4. 3.Palatini P, Casiglia E, Julius S, Pessina AC. High heart rate: a risk factor for cardiovascular death in elderly men. Arch Intern Med. 1999 Mar 22;159(6):585-92. 4.Greenland P, Daviglus ML, Dyer AR, Liu K, Huang CF, Goldberger JJ, Stamler J. Resting heart rate is a risk factor for cardiovascular and noncardiovascular mortality: the Chicago Heart Association Detection Project in Industry. Am J Epidemiol. 1999 May 1;149(9):853-62. Competing interests: None declared |
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Leslie O Simpson, retired experimental pathologist Dunedin, New Zealand 9077
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Given that blood viscosity plays an important role in most aspects of heart function, it is unlikely that the importance of resting heart rate can be assessed without recognition of the role of blood viscosity. In a Health Day interview on February 4, 2009, Professor Judith Hsia, the lead investigator of the resting heart rate study is quoted as stating, "...a higher heart rate in a woman over 50 would indicate a need for the recommended lifestyle modifications needed to prevent cardiovascular problems - a low-fat diet,lower blood pressure, avoiding obesity and more physical activity." Professor Hsia appeared to be unaware that all of the lifestyle changes have similar effects on blood rheology because they lower blood viscosity and/or increase red cell deformability. It is not surprising therefore to find in Table 1 that subjects with more than 76bpm had the highest percentages for hypertension, diabetes mellitus, current smoking, high cholesterol- requiring drugs and the lowest levels of physical activity, all of which share the common feature of increased blood viscosity. It is of some significance that Gullesbrad et al (1) should record in men in the quintile with the highest bpm, the highest levels for smoking, diabetes history,and a history of hypertension. Such changes, in both men and women are associated with higher levels of blood viscosity. While physical fitness is associated with low resting heart rate and low blood viscosity, in individuals over 50 years of age blood viscosity shows an age-related increase with an increase in resting heart rate. So in physically fit individuals the low blood viscosity and low resting heart rate implies that the reduced vascular resistance will be associated with a large ejection fraction. But in individuals with increased blood viscosity which will raise the resistance to flow,a reduced ejection fraction would require an increased heart rate to provide an adequate volume of blood. Clements et al (2) hypothesised that, "...within the normal range of resting heart rate, heart rate and left ventricular ejection fraction would be inversely correlated, etc," but made no comment about how blood viscosity changes might influence the situation. It seems that the assessment of resting heart rate could be a surrogate method of assessing blood viscosity, implying that those with high resting heart rates might benefit from a daily supplement of 6 grams of fish oil to lower blood viscosity and to increase the fluidity of red cell membranes. In a study involving 18 men, the effects of placebo or omega-3 fatty acids were assessed in a randomised cross-over study for two 4 month periods. (3) Although the omega-3 fatty acids lowered resting heart rate and improved the heart rate recovery after exercise, there were no other benefits in several other factors. To some extent the results would reflect the great predominance of docosohexanoic acid over eicosapentaenoic acid as it it is the latter acid which has been shown to benefit the flow properties of blood. But no mention was made by the authors of the published information about omega-3 fatty acids and blood flow. Because of the simple non-invasive nature of resting heart rate, the possible benefits of fish oil in those with high resting heart rates needs to be investigated. References. 1. Gullesbrad L, Wiksbrand J, Deedwania P, et al. What resting heart rate should one aim for when treating patients with heart failure with beta blockers ? J Am Coll Cardiol 2005; 45: 252-9. 2. Clements IP, Miller WL, Olson LJ. Resting heart rate and cardiac function in dilated cardiopathy. Int J Cardiol 1999; 72: 27-37. 3. O'Keefe JH, Abuissa H, Sastre A, et al. Effects of omega-3 fatty acids on resting heart rate, heart rate recovery after exercise and heart rate variability in men with healed myocardial infarctions and depressed ejection fractions. Am J Cardiol 2006; 97: 1227-30. Competing interests: None declared |
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Pascal Meier, MD University Hospital Bern, 3010 Bern, Switzerland, Steffen Gloekler, Tobias Traupe, Stefano de Marchi , Christian Seiler
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We would like to commend Hsia J. et al.(1) on their very interesting and well done study demonstrating a predictive role of heart rate (HR) on mortality which is confirming previously published observations. Despite this consistency, such observational studies generally entail the difficulty to untangle cause from association. A plausible underlying mechanism certainly would invigorate causality. Previously, authors hypothesized that increased HR could damage heart and vessels due to increased shear forces. Indeed, we strongly suggest that shear forces play an underlying role, but in the opposite direction. The common misconception of a negative effect of shear stress requires revision. Low HR comes along with increased stroke volume and prolonged diastole. The resulting increased shear stress in turn stimulates arterial growth in general and collateral growth in particular and reduces atherosclerotic progression. (2-4) These pro-arteriogenic and anti-atherogenic processes distinctively improve long-term outcome.(5) Consequently, we hypothesize that the association of outcome and HR is causal rather than casual, and it may be mediated by higher shear stress on coronary endothelial cells. However, in order to corroborate causation, interventional studies have to follow. What if we change HR long term, do we influence mortality? Trials inducing HR reduction by different means in order rule out direct or confounded influence of the intervention on outcome are meaningful. References 1. Hsia J, Larson JC, Ockene J, Sarto GE, et al. Resting heart rate as a low tech predictor of coronary events in women: prospective cohort study. BMJ 2009 338(b219 ). 2. Seiler C, Kirkeeide RL, Gould KL. Basic structure-function relations of the epicardial coronary vascular tree. Basis of quantitative coronary arteriography for diffuse coronary artery disease. Circulation 1992;85(6):1987-2003. 3. Pipp F, Boehm S, Cai WJ, Adili F, et al. Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hind limb. Arterioscler Thromb Vasc Biol 2004;24(9):1664-8. 4. Traub O, Berk BC. Laminar shear stress: mechanisms by which endothelial cells transduce an atheroprotective force. Arterioscler Thromb Vasc Biol 1998;18(5):677-85. 5. Meier P, Gloekler S, Zbinden R, et al. Beneficial effect of recruitable collaterals: a 10-year follow-up study in patients with stable coronary artery disease undergoing quantitative collateral measurements. Circulation 2007;116(9):975-83. Potential Financial Conflicts of Interest: None. Competing interests: None declared |
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Michael J Campbell, Professor of Medical Statistics Medical Statistics Group, ScHARR, University of Sheffield S1 4DA
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It is a fundamental principle in public health that one should never quote a relative risk without also giving the absolute risk1. Failure to follow this simple precept results in the weekly health scares that engage the popular press, when an increased relative risk is taken as a threat to the individual. Hsia et al2 flagrantly ignore this principle when they claim that ‘resting heart rate… independently predicts myocardial infarction or coronary death in women’. They base this assertion on a hazard ratio of 1.26 (95% CI 1.11 to 1.42) for these events in women above the top quintile for heart rate compared to women below the bottom in a cohort of women. They do not quote absolute risks. Based on some simplifying assumptions (equating hazard rate to relative risk, assuming total events in lower fifth and upper fifth is proportional to the number of subjects in these groups) I estimated that the absolute risk of myocardial infarction or coronary death in the 7.8 years of follow up for a woman to be 0.0194 for those in the top fifth, and 0.0154 in those in the bottom fifth. This equates to an absolute difference of 0.4% or a NNTH of 250 (95% CI 167 to 539). In other words, in those we deemed at a higher risk, out of 250 women only one extra woman would have an event in about 8 years. This is not what the public think of as a 'predictor'. Those in the top fifth should not be unduly concerned. 1. Campbell MJ, Machin D and Walters SJ. Medical Statistics : A Textbook for the Health Sciences. (4th Ed) Chichester: John Wiley & Sons 2007, p24 2. Hsia J, Larson JC, Ockene JK, Sarto GE, Allison MA, Hendrix SL, Robinson J, LaCroix AZ, Manson J.Resting heart rate as a low tech predictor of coronary events in women: prospective cohort study. BMJ 2009;338:b219 doi:10.1136/bmj.b219 Competing interests: None declared |
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Peter AF Watson, General Practitioner Links Medical Practice Aberdeen AB24 5AU
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I read with interest Hsia et al's(1) research on resting heartbeat in women as a low tech predictor of coronary events. One of my patients is an engineer. His mechanistic view of the heart leads him to believe that humans only have so many predetermined heart beats. When they are all used up we die. Clearly fitter healthier people have a lower resting heart rate and so live longer. 1 Hsia et al. Resting heart rate as a low tech predictor of coronary events in women: prospective cohort study. BMJ 2009; 338:b219 Competing interests: None declared |
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John Arthur Lee, Retired Consultant in Public Health 1 Lugg View Close, Hereford HR1 1JT
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The Women's Health Initiative Research Group (1) showed that resting heart rate, a low-tech and inexpensive measure of autonomic tone, independently predicted myocardial infarction or coronary death in women - previous studies had shown this association in men. This study supports the conclusion of a literature review (2) which showed that all the conventional risk factors for coronary heart disease (c.h.d.) were associated with the sympathetic nervous system (s.n.s.), which was implicated in all the mechanisms of c.h.d.; indicating that the s.n.s. played a major role in the actiology and pathogenesis of c.h.d. The Group's finding that the resting heart rate's relating to c.h.d. was independent of physical activity and conventional risk factors shows the importance of the degree of reactivity of the s.n.s. Hilton (3) has shown that there is great, individual variation in such reactivity. The Group's study also shows that there may be unidentified or unmeasured risk factors, such as psychosocial stress, including anxiety, as the authors point out, which contributed to the findings. It would be most interesting if the Group's authors were able to show the number and range of risk factors associated with the pulse rates and number and incidence of coronary events. It is known that many patients with c.h.d. do not have any risk factors. So there may be some patients with risk factors who have a low pulse rate and absence of c.h.d., and others with no recorded risk factors who have high pulse rates and develop c.h.d. The Group's study has important implications for future research, prevention and management of c.h.d. References: 1. Women's Health Research Group. Resting heart rate as a low tech predictor of coronary events in women: prospective cohort study. BMJ 2009; 338: b219 (7 March). 2. Lee JA. The role of the sympathetic nervous system in ischaemic heart disease: A review of epidemiological features and risk factors, integration with clinical and experimental evidence and hypothesis. Activitas Nervosa Superior 1983; 25: 110-21. 3. Hilton SM. The defence-arousal system and its relevance for circulatory and respiratory control. Journal of Experimental Biology 1982; 100: 159-74. Competing interests: None declared |
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Richard G Fiddian-Green, FRCS, FACS None
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In their rapid response Carlos Escobar, Rocio Echarri, and Vivencio Barrios asked whether an increase in heart rate might be a cause or effect of coronary events in women (1). It may indeed be an effect a rise in pulse rate being, from a metabolic perspective, an indication of the need to deliver more nutrient to meet the metabolic demands of the tissues at the time. A rise in blood catecholamines, a rise in fasting blood sugar and a rise in blood pressure (2) might all be interpreted in the same way. An acute coronary event might only be a cause if it compromises myocardial function to the degree that it impairs, or compounds an impairment of, the systemic energy supply/demand. But this might be highly unusual the low cardiac output syndrome being a productive, rather than a harmful endogenous response to the acute coronary event in tyhat it decreases myocaridla workload. In which case a fall in catecholamines, fasting blood sugar and even blood pressure might all be interpreted as evidence of an improvement in systemic tissue energy supply/demand rather than the reverse. If so decreasing cardiac output, or rather allowing it to fall, may be a far more desirable therapeutic objective in an acute coronary event than the conventional attempts of actively increasing it with fluids and inotropes. By increasing myocardial workload the latter might even increase the risk of myocardial failure and sudden cardiac death. 1. Women, heart rate and coronary disease. Cause or consequence? Carlos Escobar, Rocio Echarri, Vivencio Barrios (9 February 2009) 2. Systolic blood pressure -- Basile 325 (7370): 917 -- BMJbmj.com, 28 Oct 2002 [Full text]; Hypertension: product of mitochondrial dysfunction? Richard G Fiddian-Green bmj.com, 1 Nov 2002 [Full text] ... www.bmj.com/cgi/content/full/325/7370/917 Competing interests: None declared |
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William E Moody, Cardiology ST2 Trainee Solihull Hospital, B91 2JL
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I propose short-term assessment of heart rate variability (HRV) as a more reliable measure of autonomic nervous system function than measurement of resting heart rate. Whilst heart rate is an easy variable to measure it is dependent on a multitude of factors and inherently dynamic. Consequently, the assumption of the authors that heart rate is a good marker of sympathetic tone can in certain circumstances be misleading (1). The authors mention HRV only briefly in their discussion of their findings in relation to depression. HRV is largely determined by vagally mediated beat to beat variability, conventionally known as respiratory sinus arrhythmia. HRV is primarily a marker of activity in cardiac vagal motor neurons originating from the nucleus ambiguus within the brainstem. It is a powerful and independent predictor of an adverse prognosis in patients with heart disease as well as in the general population (2). Along with heart rate, it too is easy to measure, inexpensive and only minimally more invasive. HRV analysis has recently been reviewed and reliability indexes tend to improve during paced breathing (3). It is more than likely that those women with higher resting heart rates would have exhibited reduced HRV and so predict myocardial infarct or coronary death. As with heart rate, it is still unclear whether the relationship between measures of cardiac vagal control and mortality is causative or mere association. Mechanisms by which cardiac vagal activity may enhance prognosis include a decrease in myocardial oxygen demand, an attenuation in sympathetic activity and a reduced susceptibility of the myocardium to ventricular tachycardia. In animals, augmentation of cardiac vagal control by nerve stimulation or by drugs is associated with a reduction in sudden death in susceptible models. In humans, a number of drugs including ACE inhibitors and beta-blockers which have evidence for reducing mortality and sudden death in large randomised trials can also be demonstrated to increase HRV (1). References. 1. Resting heart rate as a low tech predictor of coronary events in women: prospective cohort study. Hsia J, Larson JC, Ockene JK et al. BMJ 2009; 338: b219. 2. Heart rate variability – a therapeutic target? Routledge HC, Chowdhary S, Townend JN. J Clin Pharm Ther. 2002;27: 85-92. Review. 3. Heart rate variability measures: a fresh look at reliability. Pinna GD, Maestri R, Torunski A et al. Clin Sci (Lond). 2007; 113: 131-40. Competing interests: None declared |
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Richard G Fiddian-Green, FRCS, FACS None
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It is not possible for heart failure to be present if the pCO2-gap and/or the intramucosal pH is normal (1). Neither should it be possible for it to be present if there is not a similar metabolic abnormality in the heart per se. An increase in heart rate variablilty might indeeed be a better indication of impaired myocardial function than an elevated resting rate, as William Moody suggested in his eLetter (2), especially if it is the product of an antecedent increase in amplitude of synchronised metabolic variations (3). We really do need to rethink these issues. 1. On the need to redefine heart failure. Richard G Fiddian-Green bmj.com, 23 Feb 2009 eLetter re: John E Sanderson and Gabriel W K Yip Heart failure with a normal ejection fraction BMJ 2009; 338: b52 2. So what about heart rate variability.....? William E Moody (19 March 2009) 3. SUD: product of an abnormally increased amplitude of synchronised metabolic variations? Richard G Fiddian-Green (16 November 2004)eLetter re: A M A Shehab, R J MacFadyen, M McLaren, R Tavendale, J J F Belch, and A D Struthers Sudden unexpected death in heart failure may be preceded by short term, intraindividual increases in inflammation and in autonomic dysfunction: a pilot study Heart 2004; 90: 1263-1268 Competing interests: None declared |
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