Mannose-binding lectin: an ancient molecule with new implications in myocardial infarction - Figure 1
Hypothesis of the pathophysiological mechanism of MBL in myocardial infarction. Presumably low MBL-levels result in a lower incidence of fatal arrhythmias by modulating myocardial ischaemia/reperfusion injury.
Getting to the heart of the matter: cardiac involvement in transthyretin-related amyloidosis - Figure 1
Diagnostic algorithm for suspected cardiac amyloidosis. AL, amyloidosis; ATTR, transthyretin-related amyloidosis; AV, atrioventricular; LV, left ventricular; RV, right ventricular; SSA, senile systemic amyloidosis; TTR, transthyretin.
Arrhythmogenic right ventricular remodelling in endurance athletes: Pandora's box or Achilles' heel?
The concept of exercise-induced arrhythmogenic right ventricular cardiomyopathy, and potential risk stratification techniques for sudden cardiac death. EVM, endocardial voltage mapping; LV, left ventricular; RV, right ventricular; SAECG, signal-averaged electrocardiogram; TWI, T wave inversion; VF, ventricular fibrillation; VT, ventricular tachycardia.
Unveiling wild-type transthyretin cardiac amyloidosis as a significant and potentially modifiable cause of heart failure with preserved ejection fraction
Screening and treatment paradigm for unveiling transthyretin amyloid (ATTR) as a potentially modifiable cause of heart failure with preserved ejection fraction (HFpEF). The diagnosis of TTR cardiac amyloidosis among patients hospitalized with heart failure (A) can be ascertained using technetium 99 m bone tracers (B) so that emerging therapies may be offered (C).