Ischemic Heart Disease and Acute Chest Pain - Cases

1351853 - Is the acute obstructive lesion the only culprit?

Thursday, January 26, 2023

7:00 AM – 7:50 AM

Location: Silver Pearl 3

Presenting Author(s)

SH

Siyi Huang, MD

Fellow
University of California, San Francisco, Fresno, California, United States

Primary Author(s)

SH

Siyi Huang, MD

Fellow
University of California, San Francisco, Fresno, California, United States

Co-Author(s)

AS

Ashwini Sadhale, MD

Fellow
University of California, San Francisco, Fresno, California, United States
SK

Siri Kunchakarra, MD

Assistant professor
University of California, San Francisco, Fresno
Chicago, Illinois, United States
AR

Ankit Rathod, MD

Associate professor
University of California, San Francisco, Fresno, California, United States

Description of Clinical Presentation: An 81-year-old male with history of hypertension, hyperlipidemia, and diabetes presented to the emergency room for acute onset chest pain. He denied any physical or emotional triggers. His chest pain resolved with sublingual nitroglycerin. Electrocardiogram showed dynamic but minimal ST-segment elevation in precordial leads compared to prior EKGs. Emergent coronary angiography showed a severe focal ulcerative lesion (90% stenosis) in the mid LAD (Figure 1). It was successfully re-vascularized with a drug-eluting stent. Troponin peaked at 3.5 ng/ml (normal range < 0.04 ng/ml). Transthoracic echocardiography on admission showed apical akinesis with hypercontractile bases. Left ventricular ejection fraction (LVEF) was estimated at 35%. The extent of wall motion abnormality and troponin elevation seemed discrepant to focal LAD occlusion, so cardiac MRI was obtained.

Diagnostic Techniques and Their Most Important Findings: The MRI study (GE 1.5T system) showed severe hypokinesis in the mid and apical segments with hyperdynamic basal segments (Figure 2). First-pass rest perfusion showed a small apical septal perfusion defect. A 1 cm non-perfusing mass was seen at apex. Early and late gadolinium enhancement (LGE) imaging of the mass confirmed it to be a thrombus. LGE imaging revealed subtle, faint, patchy near transmural enhancement in apical septum (Figure 3). T2 Double inversion recovery imaging did not show any evident increase in signal. MRI confirmed the diagnosis of Takotsubo cardiomyopathy (TC).

Learning Points from this Case: TC is a transient reversible left ventricular dysfunction commonly preceded by an emotional or physical stress trigger. The absence of LGE is generally believed to be one of the predominant features of TC. However, recent studies have shown that LGE can be present in some cases of TC. It may be caused by increased interstitial water content, rather than irreversible myocardial necrosis. In our patient, cine imaging showed a classic pattern of mid-apical ballooning with wall motion abnormalities extending beyond LAD artery distribution. LGE was not in a typical coronary infarct pattern, and signal intensity is lower than what is usually seen in myocardial infarction. Overall findings support the diagnosis of TC.

Distinguishing TC from acute coronary syndrome (ACS) can be challenging as the clinical presentation can often mimic each other. TC is usually considered a diagnosis of exclusion. Recent studies show that TC and ACS are not mutually exclusive and may co-exist. TC also is known to be associated the coronary dissection. In our case, we did not have IVUS imaging of LAD lesion to make such assessment. Cardiac MRI has become an important tool for diagnosing TC. Our case highlights that an acute coronary obstructive event does not always exclude TC. Moreover, cardiac MRI can detect potential complications such as thrombus, which may be underdiagnosed by echocardiography.