Reduced stress perfusion in myocardial infarction with nonobstructive coronary arteries

Background: Wilson disease (WD) causes intracellular copper accumulation in the body due to a genetic defect in the protein ATP7B. Cardiac involvement such as electrocardiographic abnormalities, rhythm abnormalities, heart failure and cardiac death have been reported, however pathophysiological mechanisms remain unclear. Objectives: This study aimed to comprehensively assess the myocardium in WD patients without cardiac symptoms using multiparametric cardiovascular magnetic resonance imaging (CMR), including quantitative stress perfusion mapping and strain analysis. Methods: WD patients (n=17, 41±16 years, 47% female) and volunteers (n=17, 39±15 years, 47% female) underwent multiparametric mapping at 1.5 T CMR including cine, native T1, native T2, adenosine stress perfusion mapping, late gadolinium enhancement (LGE), and extracellular volume (ECV) imaging. Symptoms of myocardial ischemia were quantified using Seattle Angina Questionnaire-7 (SAQ-7) and cardiovascular risk factors and medications were recorded. Results: Both stress perfusion and MPR were lower in WD patients (2.95±0.58 vs 3.67±1.01 ml/min/g, and 3.4±0.8 vs 4.4±1.9), while ECV was higher, (29±3% vs 27±2%), p<0.05 for all. Left ventricular ejection fraction (LVEF) was lower in WD patients, (56±6% vs 61±6%, p=0.02), and LV ventricular global circumferential strain (LV GCS) was higher (-18±2% vs -20±2%, p=0.005). Late gadolinium enhancement (LGE) was present in the right ventricular insertion point (RVIP) in 12/17 (71%) of the WD patients. Conclusions: In this small mechanistic study, WD patients on stable treatment without apparent cardiac symptoms have early signs of diffuse fibrosis, coronary microvascular dysfunction (CMD) and systolic dysfunction, shedding light on pathophysiological mechanisms of cardiac dysfunction in copper accumulation.

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Long-Term Coronary Microvascular and Cardiac Dysfunction Following Severe COVID-19 Hospitalization

Johansson,

Loewenstein,

Lodin

et al. 2024

Preprint

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Background: Coronavirus disease 2019 (COVID-19) can lead to long-term cardiopulmonary symptoms and is associated to coronary microvascular dysfunction (CMD). However, long-term data on CMD following severe COVID-19 are lacking. Objective: To determine long-term left ventricular (LV) function and presence of CMD after severe COVID-19, utilizing cardiovascular magnetic resonance (CMR) and stress perfusion mapping. Methods: Hospitalized COVID-19 patients underwent CMR at 10 months follow-up (1.5T Aera, Siemens Healthineers) including cine imaging, native T1 and T2, extracellular volume, and adenosine stress perfusion mapping. Clinical data were obtained from patient records. Patients were compared to volunteers without symptomatic ischemic heart disease (IHD). Results: COVID-19 patients (n=37, age 56±12 years, 76% male) and volunteers (n=22, age 51±13 years, 55% male, p=ns for both) were included. COVID-19 patients demonstrated reduced stress perfusion (2.8±0.81 vs 3.4±0.69 ml/min/g, p=0.003), impaired global longitudinal strain (GLS, -17±2 vs -19±2 %, p=0.003) and global circumferential strain (GCS, -16±3 vs -19±3 %, p=0.001). There were no differences in stress perfusion or myocardial perfusion reserve between COVID-19 patients with or without cardiovascular risk factors or cardiac symptoms. Conclusion: COVID-19 patients exhibit long-term reduced stress perfusion indicating CMD, and impaired LV function by GLS and GCS. Lack of variation in stress perfusion between patients with and without cardiovascular risk factors suggests that CMD may be a consequence of severe COVID-19, warranting further investigation to elucidate mechanisms, and guide potential therapeutic interventions.

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Reduced stress perfusion in myocardial infarction with nonobstructive coronary arteries

Cited by 4 publications

References 49 publications

No differences in native T1 of the renal cortex between Fabry disease patients and healthy subjects in cardiac-dedicated native T1 maps

No differences in native T1 of the renal cortex between Fabry disease patients and healthy subjects in cardiac-dedicated native T1 maps

Diffuse fibrosis, coronary microvascular dysfunction and systolic dysfunction in Wilson disease

Long-Term Coronary Microvascular and Cardiac Dysfunction Following Severe COVID-19 Hospitalization

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