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Association of tachycardia with morbidity and mortality: pathophysiological considerations
1Dipartimento di Medicina Clinica e Sperimentale, University of Padova, Italy.
Insights
Tachycardia, or rapid heart rate, is linked to higher mortality and metabolic issues in hypertensive individuals. Reducing heart rate may slow vascular damage, suggesting targeted therapies for autonomic control.
Area of Science:
- Cardiovascular Medicine
- Autonomic Nervous System Research
- Metabolic Syndrome
Background:
- Tachycardia is associated with increased cardiovascular and all-cause mortality.
- Hypertensive individuals with tachycardia often present with metabolic abnormalities including obesity, dyslipidemia, and insulin resistance.
- Sympathetic overactivity is implicated in both the elevated heart rate and blood pressure, as well as metabolic disturbances.
Purpose of the Study:
- To explore the link between tachycardia, sympathetic overactivity, and associated metabolic and cardiovascular complications.
- To investigate the potential of heart rate reduction in mitigating vascular damage.
- To identify preferred antihypertensive strategies for hypertensive patients with tachycardia.
Main Methods:
- Review of existing literature on tachycardia, hypertension, and autonomic dysfunction.
- Analysis of the physiological mechanisms linking adrenergic receptor stimulation to insulin resistance.
- Examination of experimental data on tachycardia-induced atherosclerosis in animal models.
Main Results:
- Sympathetic overactivity contributes to tachycardia, hypertension, and metabolic syndrome.
- Beta-adrenergic and alpha-adrenergic stimulation can induce insulin resistance.
- Tachycardia may promote atherosclerosis through hemodynamic disturbances; heart rate reduction may be protective.
Conclusions:
- Tachycardia in hypertensive patients signifies autonomic dysregulation.
- Centrally acting antihypertensive agents that reduce sympathetic outflow are recommended.
- I1-imidazoline receptor agonists show promise for managing tachycardia and associated risks.
Abstract:
An increased rate of cardiovascular and all-cause mortality has been documented in subjects with tachycardia. Hypertensive subjects with tachycardia often also exhibit overweight, higher haematocrit, plasma insulin, cholesterol, and triglyceride levels whereas high density lipoprotein (HDL) is decreased. Sympathetic overactivity seems to be responsible both for the increase in heart rate and blood pressure (BP), and for metabolic abnormalities. Excessive stimulation of beta-adrenergic receptors in the skeletal muscles can cause insulin resistance and chronic beta-adrenergic stimulation which leads to a greater proportion of fast twitch insulin-resistant fibres. Also alpha-adrenergic stimulation can cause insulin resistance through vasoconstriction and the consequent decrease in the delivery of glucose and insulin to the muscles. Experimental studies in monkeys have shown that tachycardia can also produce atherosclerotic lesions via haemodynamic disturbances, by elevating the pulsatile nature of the arterial blood flow. Conversely, a reduction of heart rate could retard the development of vascular lesions. If tachycardia in hypertension is a marker of an abnormality of the autonomic control of circulation, a centrally acting antihypertensive agent which decreases the sympathetic outflow should be preferred. Drugs with agonistic properties of the I1-imidazoline receptors of the rostral ventrolateral medulla appear particularly suitable in this respect.