Mechanism of atropine-resistant atrioventricular block during inferior myocardial infarction: Possible role of adenosine

Wesley, Robert C.; Lerman, Bruce B.; DiMarco, John P.; Berne, Robert M.; Belardinelli, Luiz

doi:10.1016/s0735-1097(86)80406-5

Cited by 88 publications

(22 citation statements)

References 24 publications

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“…Our findings support the concept that activation of adenosine receptors could cause reversible bradycardia and AV nodal block in patients with acute inferior myocardial infarction (33). Insufficient perfusion of the sinus nodal area could also chronically elevate adenosine levels and thereby contribute to chronic sinus nodal and AV nodal dysfunction (33,34).…”

Section: Discussionsupporting

confidence: 84%

Altered sinus nodal and atrioventricular nodal function in freely moving mice overexpressing the A₁ adenosine receptor

Kirchhof

Fabritz²,

Fortmüller³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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. Altered sinus nodal and atrioventricular nodal function in freely moving mice overexpressing the A1 adenosine receptor. Am J Physiol Heart Circ Physiol 285: H145-H153, 2003. First published March 13, 2003 10.1152/ ajpheart.01036.2002To investigate whether altered function of adenosine receptors could contribute to sinus node or atrioventricular (AV) nodal dysfunction in conscious mammals, we studied transgenic (TG) mice with cardiac-specific overexpression of the A 1 adenosine receptor (A1AR). A Holter ECG was recorded in seven freely moving littermate pairs of mice during normal activity, exercise (5 min of swimming), and 1 h after exercise. TG mice had lower maximal heart rates (HR) than wild-type (WT) mice (normal activity: 437 Ϯ 18 vs. 522 Ϯ 24 beats/min, P Ͻ 0.05; exercise: 650 Ϯ 13 vs. 765 Ϯ 28 beats/min, P Ͻ 0.05; 1 h after exercise: 588 Ϯ 18 vs. 720 Ϯ 12 beats/min, P Ͻ 0.05; all values are means Ϯ SE). Mean HR was lower during exercise (589 Ϯ 16 vs. 698 Ϯ 34 beats/min, P Ͻ 0.05) and after exercise (495 Ϯ 16 vs. 592 Ϯ 27 beats/min, P Ͻ 0.05). Minimal HR was not different between genotypes. HR variability (SD of RR intervals) was reduced by 30% (P Ͻ 0.05) in TG compared with WT mice. Pertussis toxin (n ϭ 4 pairs, 150 g/kg ip) reversed bradycardia after 48 h. TG mice showed first-degree AV nodal block (PQ interval: 42 Ϯ 2 vs. 37 Ϯ 2 ms, P Ͻ 0.05), which was diminished but not abolished by pertussis toxin. Isolated Langendorffperfused TG hearts developed spontaneous atrial arrhythmias (3 of 6 TG mice vs. 0 of 9 WT mice, P Ͻ 0.05). In conclusion, A 1AR regulate sinus nodal and AV nodal function in the mammalian heart in vivo. Enhanced expression of A 1AR causes sinus nodal and AV nodal dysfunction and supraventricular arrhythmias. heart rate regulation; autonomous nervous system; heart rate variability; sinus node dysfunction; atrioventricular block; atrial fibrillation

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Section: Discussionsupporting

confidence: 84%

Altered sinus nodal and atrioventricular nodal function in freely moving mice overexpressing the A₁ adenosine receptor

Kirchhof

Fabritz²,

Fortmüller³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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“…38 Based on the results of the present study, restoration of 1:1 AV conduction may not always be beneficial because the AV block can be a "protective" mechanism for the ventricles from excessive demand when O 2 supply is limited. In a recent case report by Wesley et al, 39 it was noted that in the setting of inferior myocardial infarction, reversal of 2:1 AV block by aminophylline (an adenosine antagonist) to 1:1 AV conduction was accompanied by an increase of approximately 0.5 mm in ST segment elevation (Figure 1 in reference 39). Although speculative, it is conceivable that similar to the experiments of the present study, administration of aminophylline and restoration of 1:1 AV conduction in the patient of the abovementioned case report had the efiFect of introducing an "error signal" that led to an increased O 2 demand by increasing ventricular rate and, hence, causing elevation of the ST segment.…”

Section: Discussionmentioning

confidence: 98%

Atrioventricular nodal accommodation in isolated guinea pig hearts: physiological significance and role of adenosine.

Jenkins

Belardinelli

1988

Circulation Research

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The progressive prolongation of atrioventricular node (AVN) conduction time to a new steady-state value caused by sadden and maintained increases in atrial rate is the most common form of AV nodal accommodation. This study was undertaken to 1) characterize AV nodal accommodation in isolated perfused guinea pig hearts, 2) investigate the influence of potential modulators of this phenomenon such as acetylcholine and adenosine, and 3) determine the physiological significance of AV nodal accommodation on cardiac function. Beat-by-beat changes in AVN conduction time caused by single-or multiple-step increases in atrial pacing rate were measured during control conditions and in the presence of atropine (1 fiM), propranolol (1 /uM), and the adenosine antagonist BW-A1433 (1 fiM). BW-A1433 was the only intervention that significantly reduced the cumulative and frequency-dependent prolongation of AVN conduction time but this was only observed at atrial cycle lengths £ 170 msec. In addition, BW-A1433 shortened the Wenckebach cycle length from 163 ±2 to 153 ±2 during normoxia and from 172 ±3 to 164 ±4 during mild hypoxia. In contrast, dipyridamole (1 fiM), an adenosine uptake blocker, markedly accentuated the AVN conduction time prolongation, accentuated the AV block associated with fast atrial rates, and significantly increased the Wenckebach cycle length. These effects of dipyridamole were prevented and antagonized by BW-A1433 and adenosine deaminase. When O 2 supply was limited and at the same time demand increased secondary to fast atrial pacing, the rate of adenosine release increased from a control of 125 ±27 to 580 ±54 pmol/min/g. This was accompanied by a significant prolongation in AVN conduction time that invariably progressed to AV block. Once AV block occurred, O 2 consumption decreased, O 2 supply-to-demand ratio improved and the rate of adenosine release dropped to 310 ±61 pmol/min/g. Reversal of the AV block with adenosine antagonists resulted in a decrease in O 2 supply-to-demand ratio and a severalfold increase in the rate of adenosine release. In this feedback system, adenosine signals the imbalance between O 2 supply and demand, causes AV block and, thus, reduces demand to compensate for the limited O 3 supply. On the other hand, adenosine deaminase and antagonists act as "error signals" by attenuating the effect of adenosine, whereas dipyridamole enhances the "gain" of the system by potentiating the effects of adenosine. We concluded that 1) AV nodal accommodation is an intrinsic property of the AVN that can be influenced by adenosine, and 2) under conditions of low O 2 supply-to-demand ratio, adenosine is produced as a negative feedback signal that protects the ventricles from excessive work by causing AV block. The wellrecognized dependence of AV conduction time on rate is consistent with this delay in recovery of excitability of the nodal cells. Furthermore, as also reported by Merideth et al, 1 the rate-dependency of AV transmission is cumulative, which indicates that the delayed recovery of excitab...

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“…[6][7] The AV nodal artery normally arises from the right coronary artery. 8 and the ischemic insult caused by STEMI is thought to be sufficient to cause a transient dysfunction of the conduction fibers.…”

Section: Discussionmentioning

confidence: 99%

Study of Prognosis of Atrioventricular Blocks Versus Intraventricular Blocks in Acute Myocardial Infarction

Reddy¹,

Prasad²,

Prabhakar³

et al. 2016

jemds

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Myocardial infarction is a Global epidemic, and it is as large as the new epidemic afflicting population worldwide. According to the National Commission on Macro-economics and Health, there would be around 62 million patients with Coronary Artery Disease (CAD) by 2015 in India, and of these, 23 million would be younger than 40 years of age. 1 The present study will enlighten the correlation of Atrioventricular conduction defects versus intraventricular conduction defects in acute myocardial infarction after thrombolytic era. AIMS AND OBJECTIVESTo study the prognosis of atrioventricular conduction blocks versus intraventricular conduction defects in patients with acute myocardial infarction. MATERIALS AND METHODSIt is a prospective and comparative cohort study; 72 patients admitted in RLJH diagnosed as acute myocardial infarction who are with AV conduction blocks and myocardial infarction with intraventricular conduction blocks are included in the study. That is 36 patients with acute myocardial infarction with atrioventricular conduction blocks compared with 36 patients of myocardial infarction with intraventricular conduction blocks. Seven days followup is done to assess the prognosis of AV blocks versus intraventricular conduction blocks in acute myocardial infarction. RESULTSBoth AV (75%) and intraventricular (80%) blocks (IV blocks) are more in males, but no significant difference between AV and IV blocks with respect to gender. Chest pain (86%) is the common presentation for conduction disturbances in acute Myocardial Infarction (MI). Breathlessness is more specific for intraventricular blocks in acute MI. Anterior wall (52.8%) is involved in intraventricular conduction blocks compared to AV Blocks (27.8%). Inferior wall (55.6%) is involved in AV blocks more than anterior Wall (41.7%). In Killips staging most of AV blocks presented in stage 3 compared to IV block which have less risk (Stage 1) and better prognosis. Based on mortality AV blocks have more mortality of 33.3% compared to Intraventricular blocks (8.3%) in acute Myocardial Infarction (MI). CONCLUSIONHence taking all things together AV blocks are associated with greater risk or poor prognosis compared to intraventricular blocks in acute myocardial infarction according to this present study. A cross sectional study of the nutrient intake of rural Adolescent girls was carried out in four villages

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Mechanism of atropine-resistant atrioventricular block during inferior myocardial infarction: Possible role of adenosine

Cited by 88 publications

References 24 publications

Altered sinus nodal and atrioventricular nodal function in freely moving mice overexpressing the A₁ adenosine receptor

Altered sinus nodal and atrioventricular nodal function in freely moving mice overexpressing the A₁ adenosine receptor

Atrioventricular nodal accommodation in isolated guinea pig hearts: physiological significance and role of adenosine.

Study of Prognosis of Atrioventricular Blocks Versus Intraventricular Blocks in Acute Myocardial Infarction

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