Circulation: Heart Failure
IMAGES AND CASE REPORTS IN HEART FAILURE

Serial Quantitative Assessment of Myocardial
Blood Flow With 13N-Ammonia Positron Emission
Tomography in a Symptomatic Patient With
Tachycardia-Induced Cardiomyopathy
Shiro Miura , MD, MSc; Atsutaka Okizaki , MD, PhD; Osamu Manabe, MD, PhD; Chihoko Miyazaki, MD, PhD;
Takehiro Yamashita , MD, PhD

T
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achycardia-induced cardiomyopathy (TIC) is a systolic or diastolic ventricular dysfunction resulting
from prolonged elevated heart rate, often leading toheart failure. TIC was considered reversible in achieving
heart rate control; however, reversal may not occur or becomplete.1 TIC causes coronary microvascular dysfunction and is associated with significant structural alterations suggestive of myocyte injury.2 However, evidenceof the time-course changes of microcirculation fromacute to recovery phases of TIC is limited. We report theserial quantitative assessments of myocardial blood flow(MBF) and myocardial flow reserve (MFR), assessedusing myocardial perfusion positron emission tomography (PET) in a patient with TIC.

CASE PRESENTATIONA previously healthy 74-year-old man presented withrecurrent palpitations and progressive exertional dyspnea for 3 months. On admission, his blood pressure
was 131/81 mm Hg, heart rate 122 bpm, body temperature 36.7 °C, and respiratory rate 14/min, with
99% oxygen saturation on ambient air. A 12-lead ECG
showed regular narrow supraventricular tachycardia(Figure 1A). Chest radiography revealed slight cardiac
enlargement. Transthoracic echocardiogram revealed
left ventricular (LV) ejection fraction (LVEF) of 35%

to 40% with a mildly enlarged LV cavity (LV end-diastolic dimension, 53 mm), no evident LV hypertrophy,
and normal valve function. The complete blood countand metabolic profile were normal, except for increased
NT-pro-BNP (N-terminal pro-B-type natriuretic peptide) levels (2078 pg/mL; normal <125). After careful
ECG analysis, atrial tachycardia was suspected. He washospitalized for worsening heart failure 10 days afterbeta blocker and oral anticoagulant administration. On
day 2 of hospitalization, electrical cardioversion was
successfully performed for sinus rhythm restoration(Figure 1B). Coronary computed tomography angiography showed no stenotic lesions. Cardiac magnetic
resonance showed reduced LVEF of 39% with significant LV enlargement where a mid-wall late gadolinium enhancement was present in the basal septum(Figure 2A). On day 4 of hospitalization, pharmacological stress/rest 13 N-ammonia PET using ATP infusion
showed normal findings on myocardial perfusion imaging (Figure 3A) but severely reduced MFR (0.89) andstress MBF (0.62 mL/[g·min]; Figure 4A). The patient
became asymptomatic after electrical cardioversion andwas administered oral amiodarone at discharge. Twomonths after the initial presentation, he was asymptomatic with ECG showing sinus rhythm, transthoracic
echocardiogram showing mild LV hypertrophy, andimproved LVEF of 58%. The clinical course confirmed

Key Words: cardiomyopathy ◼ heart failure ◼ perfusion ◼ tachycardia ◼ tomography

Correspondence to: Shiro Miura, MD, MSc, Department of Cardiology, Hokkaido Ohno Memorial Hospital, 2-1-16-1 Miyanosawa, Nishi-ku, Sapporo 063-0052, Japan.
Email s.miura@sap-kojk.jp
For Sources of Funding and Disclosures, see page xxx.
© 2023 American Heart Association, Inc.
Circulation: Heart Failure is available at www.ahajournals.org/journal/circheartfailure

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Blood Flow in Tachycardia-Induced Cardiomyopathy

Figure 1. ECG findings.
Initial 12-lead ECG before (A) and after(B) successful electrical cardioversion.

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the definitive diagnosis of TIC per a common definition.3 At the 12-month follow-up, he was asymptomaticwith sinus rhythm, mild LV hypertrophy, and preserved
LVEF at 70%, assessed by transthoracic echocardiogram. However, repeated PET (Figure 4B) revealed
moderately reduced stress MBF (1.33 mL/[g·min]) andMFR (1.97) with normal findings on myocardial perfusion imaging (Figure 3B). In contrast, cardiac magnetic
resonance (Figure 2B) demonstrated marked LVEF
improvement at 69% with a normalized LV size and lategadolinium enhancement in the same basal septum. At
the 18-month follow-up, he was asymptomatic; ECGshowed sinus rhythm, and transthoracic echocardiogram demonstrated a preserved LVEF at 76% with mild
LV hypertrophy. Follow-up PET (Figure 4C) revealed
further improvement in stress MBF and MFR values(2.16 mL/[g·min] and 2.48, respectively), with near-normal myocardial perfusion imaging findings (Figure 3C).
The patient was recommended to undergo genetic testing; however, the proposal was declined for economic
reasons.

DISCUSSION
This case illustrates that coronary circulation impairment
could be crucial in TIC development. Abnormal tachycardia increases myocardial oxygen consumption anddecreases diastolic duration, increasing the susceptibility
to myocardial ischemia.4 Chronic supraventricular tachycardia could lead to myocardial structure and functionchanges through reduced myocardial capillaries andMBF, increased capillary-myocyte distance and coronary vascular resistance, and impaired MFR, resulting inmyocardial injury and LV dysfunction.1,5 These findings
were consistent with ours, where stress MBF and MFR
were critically reduced in the acute phase. Additionally,
the patient showed evidence of fibrotic changes in themyocardium on cardiac magnetic resonance images,
which is uncommon and suggestive of a worse prognosis in TIC.6 One of the TIC hallmarks is the reversibility of LV dysfunction. The patient showed moderately
reduced stress MBF and MFR at the 12-month follow-up PET, and both parameters were almost normal

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echocardiographic assessments suggested that negative LV remodeling in patients with TIC persists longafter tachycardia resolution at a mean follow-up of 14months.7 Furthermore, recurrent tachycardia in patientswith a prior TIC history could lead to recurrent cardiomyopathy at a faster and more severe rate, alarming a
potential risk of sudden death.8
This is the first report outlining the serial PET and cardiac magnetic resonance findings from acute to recovery
phases beyond 1 year in a patient developing TIC. Ourfindings may elucidate the potential mechanism of TICand serial changes in micro and macro levels associatedwith coronary circulation.
ARTICLE INFORMATIONAffiliations
Department of Cardiology (S.M., T.Y.) and Department of Diagnostic Radiology(C.M.), Hokkaido Ohno Memorial Hospital, Sapporo, Japan. Department of Radiology, Asahikawa Medical University, Hokkaido, Japan (A.O.). Department of Radiology, Saitama Medical Center, Jichi Medical University, Saitama-shi, Japan (O.M.).

Sources of Funding
None.

Disclosures
None.

REFERENCES
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Figure 2. Cardiovascular magnetic resonance findings.
Vertical long axis in diastolic (top) and systolic (middle) cinecardiovascular magnetic resonance (CMR) images with lategadolinium enhancement (LGE; bottom) 16 days (A) and 12 months(B) after initial presentation. In both cases, LGE (red arrowheads) ispresent in the basal septum. LVEDVI indicates indexed left ventricular
end-diastolic volume; LVEF, left ventricular ejection fraction; andLVESVI, indexed left ventricular end-systolic volume.

at the 18-month follow-up PET. Accordingly, our casesuggested that microscopic abnormalities, reflected byreduced stress MBF and MFR, may reverse more slowly
than improvement at the clinical level. Similarly, MBF
at rest increased from the initial PET to the 18-monthfollow-up PET. Therefore, we could speculate that theserial changes in rest MBF might reflect the long-term
improvement in coronary microvascular function and themyocardial changes in hemodynamic, structural, cellular,
and neurohormonal levels.1 Supporting these notionsof slow or incomplete recovery, a previous study using

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Blood Flow in Tachycardia-Induced Cardiomyopathy

Figure 3. Myocardial perfusion imaging assessed using positron emission tomography.
Polar maps of qualitative myocardial perfusion imaging from stress/rest 13N-ammonia positron emission tomography (PET) with parameters(rest) on left ventricular function 13 days (A), 12 months (B), and 18 months (C) after initial presentation. LVEDVI indicates indexed left
ventricular end-diastolic volume; LVEF, left ventricular ejection fraction; and LVESVI, indexed left ventricular end-systolic volume.

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Figure 4. Myocardial blood flow assessed using positron emission tomography.
Quantitative assessment of myocardial perfusion with 13N-ammonia positron emission tomography (PET) 13 days (A), 12 months (B), and 18
months (C) after initial presentation. Significant improvement is observed for stress myocardial blood flow (MBF) and myocardial flow reserve(MFR) from the acute phase to the 12-month follow-up, with further improvement in both parameters at the 18-month follow-up PET. LAD
indicates left anterior descending artery; LCX, left circumflex artery; and RCA, right coronary artery.
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