Women's Heart Disease

1351740 - Stress Myocardial Blood Flow is Abnormal During Acute Takotsubo Syndrome

Wednesday, January 25, 2023

Location: E-POSTER

Presenting Author(s)

RS

Retu Saxena, MD

Cardiologist
Minneapolis Heart Institute at Abbott Northwestern Hospital, United States

Primary Author(s)

RS

Retu Saxena, MD

Cardiologist
Minneapolis Heart Institute at Abbott Northwestern Hospital, United States

Co-Author(s)

Joao Cavalcante, MD

Director, Cardiac MRI and Structural CT Labs
Minneapolis Heart Institute at Abbott Northwestern Hospital
Minneapolis, Minnesota, United States
DW

Dawn Witt, PhD

Senior Scientist
Minneapolis Heart Institute Foundation, Minnesota, United States
SS

Sarah Schwager, RN

RN
Minneapolis Heart Institute Foundation, United States
RG

Ross Garberich, MSc, MBA

Sr. Director Scientific Services
Minneapols Heart Institute Foundation, United States
GB

Gretchen Benson

Program Director
Minneapolis Heart Institute Foundation
Minneapolis, United States
OL

Opema Lohese

Research Associate
Minneapolis Heart Institute at Abbott Northwestern Hospital, Minnesota, United States
PK

Peter Kellman, PhD

Senior Scientist
National Institutes of Health, Maryland, United States
HX

Hui Xue, PhD

Director, Imaging AI Program
National Institutes of Health
Bethesda, Maryland, United States
SS

Scott Sharkey, MD

MD
Minneapolis Heart Institute Foundation, United States

Disclosure(s):

Joao Cavalcante, MD: No relevant disclosure to display

Background: Coronary microvascular dysfunction (CMD) is a proposed mechanism for takotsubo syndrome (TS). To date, it is unknown whether changes in stress myocardial blood flow (MBF) exist during acute TS presentation, their associated mechanisms, and the natural course of such abnormalities. In a proof-of-concept mechanistic study, cardiac magnetic resonance imaging (CMR) with T2 mapping and quantitative stress perfusion were used to comprehensively evaluate during the acute TS presentation and at 6-months later.

Methods: Between March and September 2021, patients who met criteria for acute TS with mid-apical regional wall motion abnormalities (WMA) and no significant coronary artery obstruction were enrolled at Allina Health Minneapolis Heart Institute at Abbott Northwestern Hospital (Minneapolis, MN). After informed consent, patients underwent comprehensive adenosine stress CMR study with cine imaging, T2-mapping, quantitative perfusion with automated in-line quantification of global and regional MBF, in addition to late gadolinium enhancement (LGE) imaging. Same protocol was repeated at 6-months from initial CMR exam to assess for interval changes

Results:

A total of 8 patients have been recruited and consented. Four participants have completed the 6 months follow up. All were women, age range 49-77 years, with emotional trigger and mild troponin elevation. CMR was performed within 3 days from presentation; left ventricular (LV) ejection fraction was 37-55% with hypokinesis in the mid-apical segments. Regional myocardial edema along with hypokinesis or akinesis in the mid-apical segments were present LGE was absent in all patients.

Global stress MBF was normal (ie: ≥ 2.0 ml/min/g) in all patients, but regional stress MBF was decreased in apical segments: basal/apex ratio ≥ 1.5 (normal=1.0) Repeat CMR at 6 months after acute presentation in these four patients have demonstrated resolution of myocardial edema, normalization of LV contractility and of Stress MBF

Conclusion:

During acute TS, regional MBF response to adenosine stress is decreased in abnormally contracting and edematous LV segments reflecting acute CMD. At 6 months after acute presentation, there was no evidence of residual CMD in this limited cohort given normalization of both global and regional myocardial blood flow, which suggests that chronic CMD is less likely to be a mechanism of acute TS. Expansion of this research study is currently underway at our institution.