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Interpreting Coronary Perfusion Endpoints: A Multidimensional Framework for Physiologic and Clinical Integration.

Aryan Manglik¹, Yanmin Qu²

¹From the Drexel University College of Medicine, Philadelphia, PA.

Cardiology in Review

|June 10, 2026

Summary

Third-generation beta-blockers like carvedilol and nebivolol have vasodilatory effects, but their human vascular impact needs clearer definition. This review suggests combining coronary flow reserve and microvascular resistance measures to better understand drug mechanisms in the human vasculature.

Keywords:

coronary flow reserve coronary microvascular dysfunction coronary physiology endothelial function index of microcirculatory resistance microvascular resistance reserve perfusion endpoints vascular resistance β-blockers

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Area of Science:

Cardiovascular Pharmacology
Human Physiology
Microcirculation Research

Background:

Third-generation beta-blockers (e.g., carvedilol, nebivolol) possess vasodilatory properties via alpha1-adrenergic antagonism and nitric oxide pathways.
Translating ex vivo and receptor-level data to in vivo human vascular effects remains challenging.
Current human studies often use composite perfusion endpoints (e.g., coronary flow reserve) influenced by multiple hemodynamic factors, limiting mechanistic insight.

Purpose of the Study:

To propose a structured framework for interpreting human vascular effects of beta-blockers.
To enhance mechanistic understanding of vasodilatory properties of third-generation beta-blockers in vivo.
To differentiate intrinsic microvascular responses from systemic influences on perfusion endpoints.

Main Methods:

Review and synthesis of existing human interventional studies on beta-blocker vascular effects.
Proposal of a combined interpretation framework for coronary flow reserve (CFR), index of microcirculatory resistance (IMR), and microvascular resistance reserve (MRR).
Context-dependent analysis across various disease states to identify dominant physiologic contributors.

Main Results:

Existing perfusion endpoints are often composite, hindering specific mechanistic attribution.
A combined framework interpreting CFR, IMR, and MRR offers a more coherent approach to understanding vasodilatory reserve utilization.
This approach aims to contextualize drug effects within specific physiological and pathological conditions.

Conclusions:

Interpreting perfusion endpoints in combination provides a more nuanced understanding of beta-blocker vascular pharmacology.
The proposed framework can improve characterization of pharmacologic vascular effects in humans.
This approach may guide future research to better distinguish intrinsic microvascular actions from systemic hemodynamic effects.