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These studies suggest that lisinopril generally reduces blood pressure without significantly affecting heart rate, although it may improve heart rate variability and sympathetic response during exercise in certain conditions.
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Lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, is widely used in the management of hypertension and heart failure. Its effects on heart rate, however, are nuanced and vary depending on the clinical context and patient population. This article synthesizes findings from multiple studies to provide a clear understanding of how lisinopril influences heart rate.
In patients with congestive heart failure (CHF) and chronic atrial fibrillation, lisinopril was found to improve peak oxygen consumption and reduce plasma norepinephrine levels during exercise, indicating a reduction in adrenergic drive. However, heart rate during exercise and ambulatory monitoring was not significantly affected by lisinopril.
A study comparing the effects of lisinopril and valsartan on autonomic nervous system activity in CHF patients found no significant differences in their impact on heart rate variability and baroreflex sensitivity. Both medications significantly reduced plasma norepinephrine levels, but valsartan had a more pronounced effect. This suggests that while both drugs modulate sympathetic activity, their influence on heart rate may be similar.
In a large multicenter study, lisinopril, both alone and in combination with hydrochlorothiazide, effectively reduced blood pressure without significantly affecting heart rate. This indicates that lisinopril can lower blood pressure while maintaining stable heart rates in hypertensive patients.
In patients with heart failure, acute administration of lisinopril resulted in significant reductions in mean arterial pressure, pulmonary capillary wedge pressure, and systemic vascular resistance. However, no significant changes in heart rate were observed, highlighting lisinopril's ability to improve hemodynamics without inducing reflex tachycardia.
In normotensive individuals, both acute and chronic administration of lisinopril reduced blood pressure without changing heart rate. Lisinopril also impaired vagally mediated reflexes, such as the diving reflex, indicating an increase in parasympathetic activity without affecting baroreflexes or sympathetic function.
In animal models, lisinopril treatment significantly increased heart rate variability (HRV) during both active and inactive periods, suggesting enhanced autonomic control of heart rate. This increase in HRV indicates improved autonomic regulation, which is beneficial for cardiovascular health.
In patients with acute myocardial infarction, lisinopril improved the sympathetic heart rate response during exercise in the early phase of the condition. This improvement was evident in the first month post-infarction, although the difference between treated and control groups diminished by the third month.
When combined with carvedilol, lisinopril significantly reduced the mean and variability of heart rate and cardiac workload compared to a combination with valsartan. This suggests that the addition of a beta-blocker like carvedilol to lisinopril therapy may offer superior benefits in reducing cardiac workload and stabilizing heart rate.
Lisinopril, as an ACE inhibitor, has a multifaceted impact on heart rate depending on the patient population and clinical context. While it effectively reduces blood pressure and improves hemodynamics in heart failure and hypertensive patients, its influence on heart rate is generally neutral, with no significant changes observed in most studies. However, in specific conditions like acute myocardial infarction, lisinopril can enhance sympathetic heart rate response during exercise. Combining lisinopril with beta-blockers may further optimize heart rate control and reduce cardiac workload.
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