Adenosine-Induced Coronary Steal Is Observed in Patients Presenting With ST-Segment-Elevation Myocardial Infarction

Muhammad Aetesam-Ur-Rahman1,2, Adam J Brown3, Catherine Jaworski4

  • 1Department of Interventional Cardiology Royal Papworth Hospital Cambridge United Kingdom.

Insights

Adenosine can cause coronary steal, reducing blood flow reserve in ST-segment-elevation myocardial infarction patients. This phenomenon is linked to better collateral circulation and higher microvascular resistance, impacting treatment effectiveness.

Area of Science:

  • Cardiology
  • Interventional Cardiology
  • Vascular Physiology

Background:

  • Adenosine is used to manage no-reflow during ST-segment-elevation myocardial infarction (STEMI) interventions.
  • Its physiological effects in the infarct-related artery (IRA) are variable, with coronary steal (reduced distal flow) a known complication facilitated by collaterals.
  • Understanding adenosine's impact on coronary flow reserve (CFR) in STEMI is crucial for optimizing treatment.

Purpose of the Study:

  • To investigate the effects of adenosine on coronary flow reserve (CFR) in patients with ST-segment-elevation myocardial infarction (STEMI).
  • To elucidate the physiological mechanisms underlying the variable response to adenosine, specifically the occurrence of coronary steal.
  • To correlate coronary steal with microvascular resistance and collateral function in STEMI patients.

Main Methods:

  • Pressure-wire assessment of the infarct-related artery (IRA) in 93 STEMI patients post-percutaneous coronary intervention.
  • Calculation of index of microvascular resistance (IMR), CFR, and collateral flow index (CFI) by pressure.
  • Assessment of collateral status using modified Rentrop grade and microvascular obstruction via cardiac MRI.

Main Results:

  • Adenosine-induced coronary steal (CFR <0.9) occurred in 20% of patients.
  • Coronary steal was associated with higher modified Rentrop scores (p<0.001) and CFI (p=0.004).
  • Patients experiencing steal had increased IMR (p=0.006) and more donor artery disease (p=0.02) compared to the hyperemic group.

Conclusions:

  • Adenosine-induced coronary steal can reduce coronary flow reserve in a significant proportion of STEMI patients.
  • Collateral function and microvascular resistance play key roles in mediating adenosine's effect on CFR.
  • These findings highlight the complex interplay of factors influencing adenosine's efficacy in STEMI interventions.

Related Concept Videos

Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations01:19

Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations

The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade the...
99
Acute Coronary Syndrome I: Introduction01:30

Acute Coronary Syndrome I: Introduction

Acute Coronary Syndrome (ACS) encompasses a spectrum of heart conditions caused by sudden obstruction of coronary arteries, typically resulting from the rupture of an atherosclerotic plaque and subsequent thrombus (blood clot) formation. This obstruction can lead to partial or complete blockage of blood flow, causing varying degrees of myocardial ischemia or infarction.ACS includes the following clinical entities:Unstable Angina (UA)Non-ST-Elevation Myocardial Infarction (NSTEMI)ST-Elevation...
198
Acute Coronary Syndrome III: Diagnostic Studies01:30

Acute Coronary Syndrome III: Diagnostic Studies

Diagnosing acute coronary syndrome or ACS begins with a thorough patient history. Notable symptoms include central, crushing chest pain radiating to the left arm, neck, jaw, or back, along with shortness of breath, sweating (diaphoresis), nausea, vomiting, dizziness, and palpitations.It is crucial to note any history of cardiac illnesses and assess risk factors, including age, gender, smoking, hypertension, diabetes, hyperlipidemia, and a sedentary lifestyle.During physical examination, vital...
58
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
2.1K
Acute Coronary Syndrome IV: Interprofessional Care01:28

Acute Coronary Syndrome IV: Interprofessional Care

IntroductionThe management of Acute Coronary Syndrome (ACS) aims to minimize myocardial damage, preserve myocardial function, and prevent complications.Initial ManagementInpatient management involves continuous cardiac monitoring, preferably in an ICU, focusing on blood pressure, serum sodium, potassium, and creatinine levels, and urine output. Ongoing pharmacologic management is crucial for stabilizing the patient.Supplemental Oxygen: Administer supplemental oxygen if oxygen saturation is...
69
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of...
1.5K