7 research outputs found
The significance of ST-elevation in aVL in anterolateral myocardial infarction: An assessment by cardiac magnetic resonance imaging
Background: Anterolateral myocardial infarction (MI) is traditionally defined on the electrocardiogram by ST-elevation (STE) in I, aVL, and the precordial leads. Traditional literature holds STE in lead aVL to be associated with occlusion proximal to the first diagonal branch of the left anterior descending coronary artery. However, concomitant ischemia of the inferior myocardium may theoretically lead to attenuation of STE in aVL. We compared segmental distribution of myocardial area at risk (MaR) in patients with and without STE in aVL. Methods: We identified patients in the MITOCARE study presenting with a first acute MI and new STE in two contiguous anterior leads from V1 to V6, with or without aVL STE. Patients underwent cardiac magnetic resonance imaging 3-5 days after acute infarction for quantitative assessment of MaR. Results: A total of 32 patients met inclusion criteria; 13 patients with and 19 without STE in lead aVL. MaR > 20% at the basal anterior segment was seen in 54% of patients with aVL STE, and 11% of those without (p = 0.011). MaR > 20% at the apical inferior segment was seen in 62% and 95% of patients with and without aVL STE, respectively (p = 0.029). The total MaR was not different between groups (44% ± 10% and 39% ± 8.3% respectively, p = 0.15). Conclusion: Patients with anterior STEMI and concomitant STE in aVL have less MaR in the apical inferior segment and more MaR in the basal anterior segment
Expert consensus document: Mitochondrial function as a therapeutic target in heart failure
Heart failure is a pressing worldwide public-health problem with millions of patients
having worsening heart failure. Despite all the available therapies, the condition carries a very
poor prognosis. Existing therapies provide symptomatic and clinical benefit, but do not fully
address molecular abnormalities that occur in cardiomyocytes. This shortcoming is particularly
important given that most patients with heart failure have viable dysfunctional myocardium,
in which an improvement or normalization of function might be possible. Although the
pathophysiology of heart failure is complex, mitochondrial dysfunction seems to be an important
target for therapy to improve cardiac function directly. Mitochondrial abnormalities include
impaired mitochondrial electron transport chain activity, increased formation of reactive oxygen
species, shifted metabolic substrate utilization, aberrant mitochondrial dynamics, and altered ion
homeostasis. In this Consensus Statement, insights into the mechanisms of mitochondrial
dysfunction in heart failure are presented, along with an overview of emerging treatments
with the potential to improve the function of the failing heart by targeting mitochondria.peerReviewe