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Mannose-binding lectin: an ancient molecule with new implications in myocardial infarction - Figure 1

Eur. Heart J. (2010), 31 (10), 1163-1164; 10.1093/eurheartj/ehq070 - Click here to view abstract

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

Eur Heart J (2013) 34 (7): 483-485; 10.1093/eurheartj/ehs238 - Click here to view abstract

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?

Eur. Heart J. (2015), 36 (30), 1955-1957, Fig 1; 10.1093/eurheartj/ehv199 - click here to view abstract

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

Eur. Heart J. (2015), 36 (38), 2595-2597, Fig 1; 10.1093/eurheartj/ehv328 - click here to view abstract

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 can be ascertained using technetium 99 m bone tracers so that emerging therapies may be offered (C).

Hypertrophic cardiomyopathy: single gene disease or complex trait?

Eur. Heart J. (2016) 37(23) doi: 10.1093/eurheartj/ehv562 - Click here to view the abstract

Penetrance of a sarcomere mutation increases with age and males tend to be diagnosed earlier compared with females. Genetic modifiers could either exacerbate or dampen the effects of the primary sarcomere mutation leading to earlier or delayed onset of clinical disease, respectively. Comorbid conditions, such as hypertension, obesity, diabetes, obstructive sleep apnoea, and sedentary lifestyle, are likely to have cumulative effects and be most influential in increasing disease penetrance and severity in older individuals. Conversely, healthy lifestyle choices and stringent adherence to treatment of comorbid disease could positively impact the natural history of HCM in sarcomere mutation carriers.

When the money is not in the bank

Eur. Heart J. (2016) 37(23) doi: 10.1093/eurheartj/ehv645 - Click here to view the abstract

Idealized relationship between phenotype, human tissue disease modeling, and translational clinical impact. ACM, arrhythmogenic cardiomyopathy; ALVC, arrhythmogenic right ventricular cardiomyopathy; ARVC, arrhythmogenic right ventricular cardiomyopathy; C-MSC; cardiac mesenchymal stromal cell; iPS, induced pleuripotent stem; LV, left ventricle; RV, right ventricle.

Proposal for a revised definition of dilated cardiomyopathy, hypokinetic non-dilated cardiomyopathy, and its implications for clinical practice: a position statement of the ESC working group on myocardial and pericardial diseases

Eur. Heart J. (2016) 37(23) doi: 10.1093/eurheartj/ehv727 - Click here to view the abstract

Description of the clinical spectrum of DCM. LV abn, left ventricle abnormality. DCM can be further classified as ND or D (non-dilation/dilation) or NH or H (non-hypokinetic/hypokinetic) or mut+ (mutation carrier) or AHA+ (anti-heart autoantibody positive) or A/CD (arrhythmia/conduction defect).

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