Although the association of HR and outcome is suggestive, it does not, by itself, prove causality. High HR also is associated with poor cardiorespiratory fitness or impaired cardiac function. Indeed, exercise capacity itself is a powerful predictor of mortality, and resting HR is lower in individuals who undertake vigorous leisure activities or participate in sports. Therefore, in recent studies significantly relating HR and mortality, adjustments have been made for the effects of physical activity and cardiac function. In the Cooper Clinic Mortality Risk Index, high HR and low cardiorespiratory fitness were both independent predictors of mortality. Relatively high HR often is found together with other cardiovascular risk factors, notably hypertension, an atherogenic blood lipid profile, blood glucose and insulin levels, and overweight. Indeed, HR correlates with the number of cardiovascular risk factors presenting in an individual.
I am less and less inclined to believe that lowering heart rate with pharmacological interventions can lower cardiac risk. As you state in your question, higher heart rates are strongly associated with reduced cardiorespiratory fitness. Simply giving a drug can't and won't change that. Recent studies do not suggest beta blockers help much for patients with CAD or recent MI; however, there is still compelling evidence that they help for patients with systolic CHF so I can't write them off completely.
lowering Heart rate by any means will have a positive impact in reducing cardiac mortality. recent studies with ivaverdine has shown more promise but ths will not improve the quality of life
Personally, I believe that HR is a useful parameter to be controlled to reduce cardiovascular risk. On the contrary, increase or decrease of HR has to be established from time to time in each individual because there are cases where HR reduction is a gold to be achieved and cases where not.
The recent guidelines of the European Society of Cardiology and the European Society of Hypertension indicate than an accelerated heart rate is considered as an independent risk factor and potentially as a target for pharmacologic therapies, especially in high-risk patients.
http://www.ncbi.nlm.nih.gov/pubmed/19615487
Changing heart rate especially important to provoke or depress arrhythmia appearing following myocardial ischemia or reperfusion. Decreasing heart rate have more protective effects against ischemia/ reperfusion induced arrhythmia. Heart rate is most effective in the development of re-entrant type of arrhythmia
The relation ship of heart rate is also linked with life span of different species as we know that the animals having more heart rate have less life span and vice versa
Heart Rate as a pharmacological target is established in HFrEF as brilliantly shown in the SHIfT study. This is related to the condition of cellular ATP depletion and norepinephrine depletion of the failing cardiomyocyte. This failing cell needs more diastolic time to recover.
The same is not necessarily true in the non-failing heart. neither beta blocking agents neither ivabradine will improve hard endpoints in angina pectoris and no heart failure or no cardiac dysfunction (beta blocker meta-analysis JACC 2014 and Signify NEJM 2014).
Frauke Gorre raised an important point on central haemodynamics: what is the effect of
heart rate reduction on arterial wave reflection. Arterial wave reflection boosts end-systolic pressure and is by far the most important vascular determinant of late-systolic wall stress (Chirinos 2013). Late-systolic wall stress (and not early-systolic or peak wall stress) triggers delayed myocardial relaxation (Chirinos 2014, Leite Moreira 1994 & Gillebert 1991) and LV hypertrophy (Kobayashi, Circ 1995). The arterial wave reflection is related in big population studies (MESA) to LV mass (Zamani 2015) and predicts CV events, incident heart failure (Chirinos, JACC 2012) and total mortality (Zamani 2014).
So, increasing HR and decreasing wave reflection could be a compensatory mechanism for increasing age-related CV stiffening.
Best regards,
Thierry
we must not forget that increase in Heart rate is a compensatory mechanism to meet out demands of anew metabolic state and the best way to treat should be correction of pathology leading for this new demand rather than augmenting the compensatory mechanism but we know some time this compensation becomes harmful and we have to address it either by Beta blocker or by other drugs
Dr Pandil, that is a good question - in a prospective cohort we have investigated the relationship between resting heart rate and mortality in subjects who had VO2max measurements performed, and we found that RHR remained a significant predictor of mortality after adjusting for level of fitness and other possible confounding factors. (http://www.ncbi.nlm.nih.gov/pubmed/23595657). This suggests that heart rate is not a mere marker of other CV risk factors. However, trials of pharmacological heart rate reduction in healthy individuals has to my knowledge not been performed and would probably be difficult to undertake for a number of reasons. Best, Magnus
The HR modulation analysis allows the clinician or researcher to know the cardiovascular status of the time of the assessment and together with the other classical tests can enable a prognosis on the cardiovascular system health. Greater HR variability is related to increased cardiac parasympathetic tone. Thus, there is greater protection against cardiac arrhythmias. In contrast, patients who have higher cardiac sympathetic tone are more likely to develop arrhythmias that can even be fatal. Therefore, assessment of cardiac autonomic modulation by HRV contributes to making treatment decisions for each patient or individual.
Yes it can. Heart rate is an important determinant of coronary blood flow. Drugs that reduce the heart rate have antianginal properties. Unlike the rest of the body, the myocardium receives its blood supply mainly in diastole. In fact during peak systole there is hardly any blood supply in certain parts of the myocardium. If there is bradycardia, the perfusion time to the myocardium is increased thus oxygen supply increases. When heart rate increases / tachycardia, the perfusion time to the myocardium is decreased. If the blood supply / oxygen supply to the heart is already compromised, say in coronary disease, this may result in further ischemia and risk of myocardial infarction..
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