Myocardial infarction (MI) following an acute coronary occlusion is a leading cause of morbidity and mortality. During revascularization, microemboli may complicate treatment and affect cardiac function. The long-term effects of microembolization are not fully elucidated.
Following an MI it is important to accurately determine the size of the infarction, as it can be used for guidance in terms of prognosis. However, in the acute setting after an MI the infarct size may be overestimated due to the inclusion of a possible reversibly injured area around the infarction, the peri-infarction zone.
In chronic MI and in non-ischemic cardiomyopathies, heterogeneous fibrotic areas have been proposed as substrate for arrhythmias which may cause sudden cardiac death (SCD). Quantification of these areas may provide better risk stratification than current guidelines.
In young people and athletes the most common cause for SCD is hypertrophic cardiomyopathy (HCM), possibly due to areas of fibrosis causing fatal arrhythmias. However, the pathophysiological mechanism behind the development of fibrosis in HCM is still unclear. Magnetic resonance imaging (MRI) can be used to assess function, perfusion and viability using late gadolinium enhancement (LGE). Therefore, this thesis investigates how MRI can be used for diagnosis, prognosis and for understanding the pathophysiological mechanisms behind ischemic and non-ischemic cardiomyopathy.
Study I showed that coronary microembolization causes long-term, regional left ventricular dysfunction and that even small microemboli, which may escape the distal protective devices, influence cardiac function.
Study II demonstrated that infarct quantification with a 2D-PSIR and a 3D-IR sequence shows good agreement in patients, which allows for the sequences to be used interchangeably. Both these LGE-sequences optimized for in vivo-use yield an overestimation of infarct size ex vivo.
Study III is an experimental study which showed that contrast-enhanced MRI overestimates myocardial infarct size compared to histopathology in the acute phase but not at seven days. This is associated with a significantly higher extracellular volume in the peri-infarction zone acutely compared to seven days later, possibly due to edema.
Study IV showed that young patients with HCM had decreased perfusion in areas with hypertrophy and even lower perfusion in LGE positive, fibrotic myocardium. The stress-induced hypoperfused regions exceed regions with fibrosis indicating that hypoperfusion precede fibrosis and may be a more sensitive marker of diseased myocardium.
Finally, Study V demonstrated that a heterogeneous LGE borderzone, quantified by two different algorithms, predicts appropriate ICD-therapy to a larger extent than ejection fraction, total, and core LGE size.
- Clinical Physiology (Lund)
- Carlsson, Marcus, Supervisor
- Arheden, Håkan, Supervisor
- Engblom, Henrik, Supervisor
- Liuba, Petru, Supervisor
|Award date||2015 May 13|
|Publication status||Published - 2015|
Place: Föreläsningssal 3, Skåne University Hospital, Lund
Name: Bluemke, David
Affiliation: National Institutes of Health, Bethesda, MD, USA
- Respiratory Medicine and Allergy
- Cardiac and Cardiovascular Systems
- Magnetic resonance imaging
- myocardial infarction
- hypertrophic cardiomyopathy