Autonomic Disturbance at Onset of Acute Myocardial Infarction

Webb, S. W.; Adgey, A. A. J.; Pantridge, J. F.

doi:10.1136/bmj.3.5818.89

Cited by 402 publications

(124 citation statements)

References 21 publications

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“…52 The activation of parasympathetic reflexes appears to have a protective effect. In experimental models depressed HRV was shown to distinguish effectively between subjects at high and low risk of developing lethal arrhythmiass3- 54 Since the first clinical observation in 1978 that the diminished respiratory sinus arrhythmia is associated with an excess of in-hospital mortality,55 multiple large-scale clinical studies have appeared defining the role of HRV in the prediction of arrhythmic events after acute myocardial More important, the predictive value of HRY has been shown to be independent of other risk factors used in the process of risk stratification, such as LV ejection fraction, increased ventricular ectopic activity.…”

Section: Risk Stratification After Myocardial Infarctionmentioning

confidence: 99%

Clinical relevance of heart rate variability

Kautzner

1997

Clinical Cardiology

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Summary: Heart rate variability (HRV) has recently become a popular noninvasive research tool in cardiology. Clinical assessment of HRV is frequently based on standard long-term ambulatory electrocardiograms, whereas physiologic studies employ spectral analysis of short-term recordings under controlled conditions. From a general point of view, HRV can be used in clinical practice to estimate (1) the integrity of cardiac autonomic innervation, (2) the physiologic status of cardiac autonomic activity, and (3) the vulnerability to various cardiac arrhythmias resulting from autonomic imbalance. Clinical relevance of HRV has been clearly demonstrated in only two clinical conditions: (1) impaired HRV can be used alone or in a combination with other factors to predict risk of arrhythmic events after acute myocardial infarction, and (2) decrease in HRV is a useful clinical marker for evolving diabetic neuropathy. Substantial advances of our knowledge are required to establish and promote clinical applications in other areas of clinical medicine. To accomplish this task, proper hypotheses should be studied and appropriate techniques selected.

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Section: Risk Stratification After Myocardial Infarctionmentioning

confidence: 99%

Clinical relevance of heart rate variability

Kautzner

1997

Clinical Cardiology

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“…Our data are in good agreement with experimental and clinical observations that sympathetic nerve terminals are preferentially distributed to the anterior wall of the left ventricle. 26 Our hypothesis of organ-specific norepinephrine release in anterior AMI and IHD associated with electrical instability seems to be further substantiated by comparison of relative increases in plasma epinephrine and norepinephrine concentrations in the clinical situations studied. Whereas relative increases in epinephrine levels were significantly higher than those in norepinephrine levels in patients with chronic IHD and posterior or posterolateral myocardial infarction, in patients with anterior or anterolateral infarction and all forms of IHD associated with electrical instability, the relative increases in norepinephrine and epinephrine levels were comparable.…”

Section: Discussionmentioning

confidence: 74%

Plasma Catecholamines and Ischemic Heart Disease

Slavikova

Kuncová

Topolčan

2007

Clinical Cardiology

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SummaryPlasma levels of norepinephrine and epinephrine were measured in 84 patients aged 56 ± 9 (mean ± SD) years with chronic ischemic heart disease (IHD), anterior acute myocardial infarction (AMI), posterior AMI, acute or chronic IHD associated with various types of electrical instability and in the control subjects. During the first day of hospitalization, plasma epinephrine levels were higher in patients with AMI in both localizations and chronic IHD in comparison with control values. There were no significant differences in plasma epinephrine levels among these groups of patients. However, in the same time period, plasma norepinephrine concentrations in patients with chronic IHD and posterior AMI did not differ from the control values; in patients with anterior AMI they reached by ∼ 60% higher values than in the control group. Moreover, all myocardial lesions showing different types of electrical instability were associated with increased plasma levels of both norepinephrine and epinephrine. In conclusion, high plasma levels of epinephrine may result from sympathoadrenal activation. High plasma levels of norepinephrine in patients with anterior AMI and no change in patients with posterior AMI suggest a rather myocardial than an extramyocardial origin of plasma norepinephrine level in anterior AMI. Norepinephrine released from the ischemic area might contribute to the electrical instability of the myocardium and generation of dysrrhythmias.

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“…During ischemia, parasympathetic nerves are activated (1,2), and the release of ATP or adenosine from cardiac tissues is increased (3,4). ACh, ATP and adenosine acti vate muscarinic, P2-purinergic and P1-purinergic receptors, respectively, and they generally decrease the automaticity of the sinus node and cardiac contractility (5)(6)(7).…”

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confidence: 99%

Effects of Glibenclamide on Negative Cardiac Responses to Cholinerg and Purinergic Stimuli and Cromakalim in the Isolated Dog Heart.

1994

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ABSTRACT-We investigated the effects of an ATP-sensitive K+ channel blocker, glibenclamide, on the negative chronotropic and inotropic responses to intracardiac parasympathetic nerve stimulation, acetyl choline (ACh, a muscarinic receptor agonist), ATP (a P2-purinergic receptor agonist), adenosine (a P1-purinergic receptor agonist) and cromakalim (a potassium channel opener) in the isolated, blood-perfused canine right atrium or left ventricle. A high dose of glibenclamide (3 ttmol) did not affect the negative chronotropic and inotropic responses to parasympathetic stimulation (frequencies of 1 30 Hz), although it slightly but significantly attenuated the negative cardiac responses to exogenous ACh (0.3 -10 nmol). Furthermore, adenosine (0.03 0.3 umol)-induced negative chronotropic and inotropic responses were significantly in hibited by glibenclamide (3 pmol), but ATP (0.01-1 pmol)-induced negative cardiac responses were not affected. A cumulative administration of cromakalim (0.01-1 pcmol) dose-dependently caused much greater decreases in the contractile force of atrial and ventricular muscles than in sinus rate. Glibenclamide (0.3 3 ,umol) similarly blocked the negative chronotropic and inotropic responses to cromakalim in a dose-depend ent manner. These results suggest that glibenclamide modifies the negative cardiac responses to parasym pathetic activation both in pre and postjunctional sites and the responses to adenosine but not to ATP at K+ channels in the dog heart, although the modifications are minor under physiological conditions.

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Autonomic Disturbance at Onset of Acute Myocardial Infarction

Cited by 402 publications

References 21 publications

Clinical relevance of heart rate variability

Clinical relevance of heart rate variability

Plasma Catecholamines and Ischemic Heart Disease

Effects of Glibenclamide on Negative Cardiac Responses to Cholinerg and Purinergic Stimuli and Cromakalim in the Isolated Dog Heart.

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