Ventricular premature depolarizations triggered by incremental dose isoproterenol infusion: common electrocardiographic features

Rivas, Núria Muñoz; Dhruvakumar, Sandhya; Mainigi, Sumeet K.; Smith, Tanya; Gerstenfeld, Edward P.; Marchlinski, Francis E.

doi:10.1007/s10840-008-9333-z

Cited by 3 publications

(2 citation statements)

References 26 publications

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“…In vivo, sympathetic imbalance and increased adrenergic drive are thought to underlie the PVCs that initiate post-MI arrhythmias, and adrenergic stimulation increases PVC incidence after MI (Rivas et al 2009). After MI, cardiac innervation undergoes extensive remodelling with denervation in the scar and partial denervation and nerve re-growth or sprouting in the peri-infarct region (Cao et al 2000;Rajendran et al 2016).…”

Section: Introductionmentioning

confidence: 99%

Altered adrenergic response in myocytes bordering a chronic myocardial infarction underlies in vivo triggered activity and repolarization instability

Dries

Amoni

Vandenberk

et al. 2020

The Journal of Physiology

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Ventricular arrhythmias are a major complication after myocardial infarction (MI), associated with sympathetic activation. The structurally heterogeneous peri-infarct zone is a known substrate, but the functional role of the myocytes is less well known. r Recordings of monophasic action potentials in vivo reveal that the peri-infarct zone is a source of delayed afterdepolarizations (DADs) and has a high beat-to-beat variability of repolarization (BVR) during adrenergic stimulation (isoproterenol, ISO). r Myocytes isolated from the peri-infarct region have more DADs and spontaneous action potentials, with spontaneous Ca 2+ release, under ISO. These myocytes also have reduced repolarization reserve and increased BVR. Other properties of post-MI remodelling are present in both peri-infarct and remote myocytes. r These data highlight the importance of altered myocyte adrenergic responses in the peri-infarct region as source and substrate of post-MI arrhythmias.

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Section: Introductionmentioning

confidence: 99%

Altered adrenergic response in myocytes bordering a chronic myocardial infarction underlies in vivo triggered activity and repolarization instability

Dries

Amoni

Vandenberk

et al. 2020

The Journal of Physiology

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“…Nuria Rivas et al demonstrated that during isoproterenol infusion (a condition simulating the high adrenergic tone which occurs in acute MI patients) the most common site of origin of premature ventricular beats is RVOT [9]. Another possible mechanism to explain the RVOT origin of ventricular ectopic beats in this patient is the presence of myocardial ischemia due to severe right coronary ostial lesion, which usually gives off the conus arteriosus artery to supply blood to the RVOT.…”

Section: Discussionmentioning

confidence: 99%

Paroxysmal Atrial Fibrillation Triggered By A Monomorphic Ventricular Couplet In A Patient With Acute Coronary Syndrome

Mattia¹,

Brieda²,

Dametto³

et al. 2012

Indian Pacing and Electrophysiology Journal

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Atrial fibrillation is a common arrhythmia in patients suffering from acute myocardial infarction, however its pathophysiological mechanisms are not fully understood. We describe the unusual case of a 76-year old woman admitted for non-ST-segment elevation myocardial infarction, who developed multiple episodes of paroxysmal atrial fibrillation triggered by monomorphic ventricular couplets. Beta-blocking and amiodarone therapy resulted efficacious in preventing arrhythmic recurrences. We then discuss the possible arrhythmogenic mechanisms, with special emphasis on the unique electrophysiological, hemodynamic, cellular and anatomical milieu created by acute myocardial ischemia.

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Clarifying the Definition of Non–Pulmonary Vein Triggers of Atrial Fibrillation

Marchlinski

Tschabrunn

Kubala

2019

JACC: Clinical Electrophysiology

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Ventricular premature depolarizations triggered by incremental dose isoproterenol infusion: common electrocardiographic features

Abstract: Adrenergically mediated VPDs are frequent in patients without structural heart disease or VT and tend to originate from a few anatomic sites.

Cited by 3 publications

References 26 publications

Altered adrenergic response in myocytes bordering a chronic myocardial infarction underlies in vivo triggered activity and repolarization instability

Altered adrenergic response in myocytes bordering a chronic myocardial infarction underlies in vivo triggered activity and repolarization instability

Paroxysmal Atrial Fibrillation Triggered By A Monomorphic Ventricular Couplet In A Patient With Acute Coronary Syndrome

Clarifying the Definition of Non–Pulmonary Vein Triggers of Atrial Fibrillation

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